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Studies from this and other laboratories have shown that interleukin-1 alpha (IL-1 alpha) stimulates corticosterone and prostaglandin (PG) release from primary cultures of rat adrenal cells. A previous report from our laboratory (1) indicated involvement of the alpha-adrenergic system in IL-1 alpha-stimulated corticosterone secretion from primary cultures of rat adrenal cells. The present experiments were conducted to determine the role of catecholamines and eicosanoids in IL-1-stimulated corticosterone release from primary rat adrenal cells. Primary adrenal cells were incubated for 24 h at 37 C with IL-1 alpha (10 nM), medium, or the appropriate agonist. After incubation, the supernatant was removed and assayed for epinephrine, prostaglandin E2 (PGE2), and corticosterone concentrations. At this time, untreated adrenal cells were fixed for immunohistochemical staining with a specific antirat tyrosine hydroxylase antibody. The results indicate that the primary adrenal cells contained 3.1 +/- 0.45% tyrosine hydroxylase-positive cells. On the ultrastructural level, the chromaffin cells were found to be in direct cellular contact with cortical cells. IL-1 alpha significantly increased (P0.05) epinephrine, PGE2, and corticosterone levels above those in medium-treated controls from primary adrenal cells. In the presence of the alpha-adrenergic antagonist phentolamine (10 microM), IL-1 alpha-stimulated (P0.05) corticosterone release was inhibited, whereas IL-1 alpha-induced PGE2 release was not affected. Conversely, the presence of the cyclooxygenase inhibitor indomethacin (10 microM) significantly inhibited IL-1 alpha-induced PGE2 secretion without altering the effect of IL-1 alpha on corticosterone release. Inhibitors of the 5-lipoxygenase system (10 microM CGS 8518) and the lipoxygenase and cytochrome P450 monooxygenase systems (10 microM nordihydroguaiaretic acid) did not effect IL-1 alpha-induced corticosterone or PGE2 release. These observations indicate that IL-1 alpha stimulates corticosterone release through an alpha-adrenergic mechanism that is independent of PGE2 release from primary rat adrenal cells.

Interleukin-1 (IL-1) has been shown to stimulate corticosterone release from the adrenal gland directly, and indirectly through activation of the hypothalamic-pituitary-adrenal axis. The aim of this paper was to determine whether IL-1-stimulated corticosterone release occurs indirectly through the local release of catecholamines from the rat adrenal gland. To accomplish this, experiments were conducted on both quartered rat adrenal glands and primary cultures of dispersed adrenal cells. Incubation of quartered adrenals with adrenocorticotropic hormone (ACTH, 10(-12) to 10(-8) M) or IL-1 beta (10(-12) to 10(-8) M) resulted in dose-dependent increases (P less than 0.05) in corticosterone release. Corticosterone release stimulated by 10(-8) M doses of ACTH and IL-1 beta began to rise 30 min after incubation and peaked at 2 h. In primary cultures of adrenal cells, IL-1 alpha and IL-1 beta elevated corticosterone release after a 24-h incubation period. ACTH elevated corticosterone levels at 4 and 24 h. The stimulatory effect of IL-1 on corticosterone release was mimicked by epinephrine (10(-6) M), and was selectively blocked by the alpha-adrenergic antagonist phentolamine (10(-5) M). The beta-adrenergic antagonist propranolol (10(-5) M) did not change IL-1-induced corticosterone release. Neither phentolamine nor propranolol had an effect on ACTH-stimulated corticosterone release. Both IL-1 alpha and IL-1 beta significantly increased (P less than 0.05) epinephrine levels after a 24-h incubation period compared with media-treated controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Out of a total of 246 food samples of animal origin screened for isolation of Aeromonas spp., 33 (13.41%) were positive for these organisms. Maximum positivity was shown by the samples from fish (28.57%), followed by poultry meat (16.67%), poultry eggs (12.50%), goat meat (12%), buffalo meat (7.69%) and cow milk (5.56%). A. hydrophila was the predominant species (51.52%) followed by A. sobria (39.39%) and A. caviae. Of these, 70.59% A. hydrophila, 69.23% A. sobria and 33.33% A. caviae showed enterotoxigenic reaction in mouse paw oedema test.

Bats are the most abundant and most widely distributed mammals on the Earth after humans. Except Antarctica and some small remote islands, they are prevalent worldwide. Although the actual role played by bats as reservoir or in disseminating zoonoses is still enigmatic a multitude of zoonotic diseases are known to be associated with bats. Such diseases including viral, bacterial, parasitic, fungal and rickettsial diseases, reported from all over the world including India have been briefed in this article as an informative approach because dramatically increased and diversified human activities during the last few decades perturbing natural ecosystems are enough to compel public health personnel to have an investigative look at these flying mammals.

Objective—To correlate substance P content of synovial fluid with prostaglandin E2content, radiographic evidence of joint abnormality, and anatomic location of the joint for normal and osteoarthritic joints of horses.Sample Population—Synovial fluid from 46 normal joints in 21 horses and 16 osteoarthritic joints in 10 horses.Procedure—Normal and osteoarthritic joints were identified by clinical and radiographic examination, by response to nerve blocks, during scintigraphy or surgery, or by clinicopathologic evaluation. Substance P and prostaglandin E2contents of synovial fluid were determined by radioimmunoassay. Radiographs of joints were assigned a numeric score reflecting severity of lesions. Joints were assigned a numeric score reflecting anatomic location.Results—Median concentrations of substance P and prostaglandin E2 were significantly increased in osteoarthritic joints, compared with normal joints. A significant correlation was found between concentrations of substance P and prostaglandin E2in synovial fluid, but a correlation was not detected between substance P concentration in synovial fluid and anatomic location of the joint or between radiographic scores of osteoarthritic joints and concentrations of substance P or prostaglandin E2.Conclusions and Clinical Relevance—A correlation existed between concentrations of substance P and prostaglandin E2in synovial fluid obtained from normal and osteoarthritic joints. However, content of substance P in synovial fluid cannot be predicted by the radiographic appearance of the joint or its anatomic location. Substance P and prostaglandin E2may share an important and related role in the etiopathogenesis of osteoarthritis, lending credence to the importance of neurogenic inflammation in horses. (Am J Vet Res2000;61: 714–718)

In experimental diabetes, diastolic dysfunction of the left ventricle has been associated with collagen-linked glycation. To determine whether less severe hyperglycemia may have similar effects, we gave alloxan to mongrel dogs (group 2) to induce impaired glucose tolerance (IGT) for comparison with normal subjects (group 1). After 6 months, hemodynamic studies were performed in the anesthetized animals. Basal heart rate, aortic pressure, and ejection fraction were comparable in the two groups, but calculated chamber stiffness was increased in group 2, associated with a reduced end diastolic volume and increased pressure. During infusion of dextran, the volume and pressure responses were similarly abnormal in group 2. In the myocardium, the collagen concentration rose with an increased interstitial distribution histologically. To assess glycation, collagen was extracted, digested with collagenase, and measured for fluorescence. Advanced glycation end products were increased in group 2 to 10.6 +/- 1.6 vs. 6.9 +/- 0.7 fluorescent units (FU)/mg collagen in group 1 (P < 0.01). To assess whether this could be pharmacologically prevented, we administered enalapril to inhibit ACE during the 6 months of glucose intolerance to group 3. This resulted in normal glycation and significant reduction in chamber stiffness increment. We gave group 4 animals aminoguanidine daily for 6 months, which prevented abnormal collagen glycation and chamber stiffness. Thus, in animals with IGT, collagen-linked glycosylation appeared to be a major factor affecting diastolic function and was shown to be amenable to pharmacological intervention.

Aeromonas spp. possess a number of virulence properties which are considered responsible for intestinal and extra-intestinal infections in human beings and also for a wide variety of infections in animals. The paper discusses current status of colonization and toxic factors of Aeromonas spp., especially in relation to food and biochemical markers. Future research needs are also identified.

A recent study from this laboratory [A. R. Gwosdow, N. A. O'Connell, and A. B. Abou-Samra. Am. J. Physiol. 263 (Endocrinol. Metab. 26): E461-E466, 1992] showed that the inflammatory mediator interleukin-1 alpha (IL-1 alpha) stimulates catecholamine release from primary cultures of rat adrenal cells. The present studies were conducted to determine whether 1) IL-1 alpha stimulates catecholamine/dopamine release from the adrenal medullary cell line PC-12 and 2) the adenosine 3',5'-cyclic monophosphate (cAMP)-protein kinase A (PKA) pathway is involved in IL-1 alpha-induced dopamine release from PC-12 cells. The results indicate that IL-1 alpha significantly (P < 0.05) elevated dopamine release after a 24-h incubation period. IL-1 alpha did not stimulate cAMP accumulation at any time period between 5 min and 2 h. In contrast, forskolin-treated cells elevated (P < 0.05) intracellular cAMP levels and increased dopamine release. Because IL-1 alpha did not affect cAMP accumulation, the effect of IL-1 alpha on PKA activity was investigated. IL-1 alpha increased (P < 0.05) PKA activity at 15 and 30 min and returned to control levels by 1 h. Forskolin also increased (P < 0.05) PKA activity. The type of PKA activated (P < 0.05) by IL-1 alpha was type II PKA. In contrast, forskolin activated (P < 0.05) type I and type II PKA. Inhibition of PKA with the PKA inhibitor H-8 blocked PKA activity and dopamine secretion by both IL-1 alpha and forskolin in PC-12 cells. These observations demonstrate that 1) IL-1 alpha stimulated dopamine release from PC-12 cells by activating PKA, 2) the mechanism of IL-1 alpha activation of PKA does not involve detectable increases in intracellular cAMP accumulation, and 3) IL-1 alpha activates type II PKA, which is used by IL-1 alpha to stimulate dopamine secretion from PC-12 cells.

Conventional plate ML-ELISA technique for diagnosis of recent cases of amoebiasis was converted into a simple polyvinyl chloride strip multilayer-enzyme linked immunosorbent assay (PVC strip ML-ELISA). This report details the development and preliminary characterization of the PVC strip ML-ELISA method for Entamoeba histolytica antigen detection in human fecal samples. In addition, we evaluated the relative efficacies of the PVC strip ML-ELISA and the conventional plate ML-ELISA methods by screening different categories of amoebiasis patients and other intestinal parasites. A significant correlation was found (P less than 0.01) between the two assay methods with reference to sensitivity and specificity of detecting E. histolytica antigens. However, with reference to operational case and economy, the PVC strip ML-ELISA may be performed even by paramedical technical personnel under field conditions.

Many studies have indicated that nitrous oxide (N2O) exposure results in specific effects on the reproductive system, some of which are antigonadotropic. The neurochemical events regulating the pituitary-gonadal axis are probably influenced by N2O, but precise documentation is lacking. The effects of exposure to 30% N2O in air on the brain tissue concentrations of luteinizing hormone releasing hormone (LHRH), substance P (SP), met-enkephalin, and beta-endorphin and on beta-endorphin concentrations of the pituitary gland are described in this study. Female rats were exposed to either N2O or air for 8 hr a day over one estrous cycle, and the brain and pituitary tissues were collected and processed. Neuropeptide concentrations were measured by specific radioimmunoassays. Exposure to N2O resulted in significant elevation of LHRH in the preoptic area, with a concomitant decrease in SP. The SP concentration of the medial basal hypothalamus was significantly elevated in N2O-exposed animals. Exposure to N2O resulted in significant increases in met-enkephalin in the brainstem area and beta-endorphin in the pituitary. These results suggest that exposure to N2O alters the interactive neural system activity regulating gonadotropin secretion from the pituitary. The significance of increased met-enkephalin in the brainstem of N2O-exposed animals is not known.

White leghorn chickens, when infected with repeated doses of Ancylostoma caninum larvae, expel the larvae at a faster rate than when infected with a single dose. This suggests that the initial dose induces some resistance in the host. An initial dose of 1000 and 2000 larvae, followed by a 2nd dose of the same order, induces resistance in the alimentary tract causing the entire larval burden either to migrate to other tissues (organs) or to be expelled in 24 h.

A study was carried out to determine the involvement of dopaminergic system in opioid-induced cardiovascular responses in the dogs. The study population consisted of 32 mongrel dogs of either sexes. The results show that morphine given in small dose (2 mg/kg I.V.) causes significant fall in blood pressure. The results also show that there is involvement of dopaminergic system in opioid-induced vasomotor responses in dogs. Partial blockade of the parenterally induced hypotensive response of morphine by haloperidol given centrally induced hypotensive responses of morphine by haloperidol given centrally in doses, which are too low to be effective by the peripheral route, strongly favours the involvement of central dopaminergic system in the morphine-induced hypotensive responses. The results also show that the hypotensive response of morphine was almost completely blocked after naloxone pretreatment by central route.

Vibrio cholerae serotypes other than I have come to be recognised as an important aetiological agent of choleraic diarrhoea and a few of them have been shown to ben enterotoxigenic in experimental models. This study was taken up with strains belonging to all the known 59 serotypes. Live cells and culture filtrates of all the strains could cause accumulation of fluid in rabbit ileal loops. However, eleven strains did so after 1-2 serial passages in rabbit gut. All the culture filtrates could also cause increased vascular permeability. The toxin was found to be heat and pH labile. The pattern of time course of fluid accumulation in ileal loop and negative suckling mouse assay indicated that the enterotoxin was heat labile. Reduction of fluid outpouring by chlorpromazine but not by synthesis and receptor blockers of prostaglandin and 5-hydroxytryptamine indicated that the toxin may act through mediation of cAMP. All the 10 strains tested were negative in Sereny's test indicating lack of invasive capacity of these organisms.

Two hundred one-day-old male white leghorn chikens (Gallus domesticus) divided into 4 groups were inoculated with a single dose of 500, 1000, 2000 or 4000 filariform larvae of Ancylostoma caninum. Larval recoveries were made from different tissues at intervals from 4 hours to 72 hours after infection. Larval migration in the heart took place within 4 hours in all the groups except group A with 500 larvae and in thoracic muscle at 8 hours. Larvae also migrated into liver, lungs and neck muscle within 12 hours and into leg muscle at 18 hours. No larvae were recovered from the muscles after 72 hours of infection. Larvae did not migrate into kidney, spleen and central nervous system throughout the experimental period.

Group 'F' vibrios are a recently recognised group of bacteria that have been isolated from cases of diarrhoea and a variety of sources in the environment. They have been shown to cause accumulation of fluid in rabbit gut loops. The enterotoxic factor was found to be heat-labile as evidenced by heat treatment, time course of fluid accumulation and negative suckling mouse assay. It was associated with cytotoxic factor(s). These organisms were seen to be lacking in invasive capacity. Prostaglandins and 5-hydroxytryptamine were found to play no role in causation of fluid outpouring into the loops but chlorpromazine was found to inhibit the fluid outpouring completely thereby indicating that the enterotoxin may act through mediation of cyclic AMP.