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Biomedical subjects

C Lombard

Publications and source records attributed to C Lombard.

At least 73 records · Page 4Linked to original sources
PubMed1989

Influence of bacterial toxins and forskolin upon vasopressin-induced inositol phosphate accumulation in WRK 1 cells.

The accumulation of inositol phosphates in WRK 1 cells, stimulated with a range of vasopressin concentrations, was diminished by prior exposure to cholera toxin or forskolin, whilst that observed in the presence of maximal concentrations of the hormone was enhanced in pertussis-toxin-treated cells. In the presence of [32P]NAD+, both cholera toxin and pertussis toxin provoked the labelling of peptides with approximate Mrs of 45,000 and 41,000 respectively in the membranes of WRK 1 cells. Exposure to cholera toxin or forskolin for 15-18 h enhanced cyclic AMP accumulation in these cells. The concentrations of these agents which provoked half-maximal cyclic AMP accumulation were similar to those required to diminish receptor-mediated inositol phosphate accumulation by 50%. In contrast, half-maximal ADP-ribosylation of the 45,000Mr peptide needed 100-fold greater concentrations of the toxin than were effective in provoking half-maximal inhibition of inositol phosphate accumulation. Cholera toxin or forskolin also reduced the maximal specific binding, to intact WRK 1 cells, of both [3H][Arg8]vasopressin and the V1a antagonist [3H][beta-mercapto-beta,beta-cyclopentamethylenepropionic acid,O-methyl-Tyr2, Arg8]vasopressin. The kinetics for the loss of this binding capacity following cholera-toxin treatment were very similar to those describing the diminution of vasopressin-stimulated inositol phosphate accumulation in the same cells.

Adenosine Diphosphate↗
PubMed1989

Diagnostic value of ascites adenosine deaminase in tuberculous peritonitis.

The value of ascitic fluid adenosine deaminase activity in distinguishing tuberculosis from other causes of ascites was examined in a retrospective study of 41 patients with bacteriologically confirmed tuberculous peritonitis and 41 control patients, matched for age and sex, with ascites of other causes (12 alcoholic cirrhosis, 5 cryptogenic cirrhosis, 12 malignant disorders, 3 pancreatitis, and 9 miscellaneous causes). The mean ascites adenosine deaminase activity was 99.8 (SD 49.1) in tuberculous patients and 14.8 (8.4) U/l in control patients (p less than 0.0001). A cutoff of 32.3 U/l had a sensitivity of 95% and specificity of 98% in distinguishing between the two groups. In a subsequent prospective study of 64 patients with ascites, 11 were found to have tuberculosis. Of the others, 23 had cirrhosis (18 alcoholic, 5 cryptogenic), 17 malignant disorders, 3 pancreatitis, 5 cor pulmonale, 3 congestive cardiac failure, 1 systemic mastocytosis, and 1 renal failure and hypothyroidism. The mean ascites adenosine deaminase activity was 112.6 (45.0) U/l in the patients with tuberculous ascites and 16.3 (36.7) U/l (p less than 0.0001) in those with ascites of other causes. In this study, adenosine deaminase had a sensitivity of 100% and specificity of 96% in discriminating tuberculosis from other causes of ascites. These findings suggest that the ascitic fluid adenosine deaminase activity may be used to identify patients in whom the diagnosis of abdominal tuberculosis must be pursued.

Adenosine Deaminase↗
PubMed1989

Properties of membranous phospholipase C from WRK1 cell: sensitivity to guanylnucleotides and bacterial toxins.

As previously described, WRK1 plasma membrane possesses a vasopressin-sensitive phospholipase C [G. Guillon et al., 1986, FEBS Lett. 196, 155-159]. In the present study, we examined the sensitivity of this enzyme to guanylnucleotides. GTP gamma S induces a time- and dose-dependent stimulation of Ins(1,4,5)P3 and Ins(1,4)P2 accumulation. No accumulation of InsP1, Ins(1,3,4)P3 or Ins(1,3,4,5)P4 occurred under similar conditions. Gpp(NH)p produced the same effect but was less potent. GTP and a nonhydrolyzable analogue of ATP, App(NH)p, were without effect. Calcium also stimulated the phospholipase C activity in a time- and dose-dependent manner. In the absence of calcium, the activity of GTP gamma S was considerably reduced. Physiological calcium concentrations (between 10(-8) and 10(-7) M), allowed maximal GTP gamma S stimulation of phospholipase C activity. In this system, the presence of vasopressin alone did not generate inositol phosphate accumulation. However, this hormone: (i) reduced the lag-time observed during GTP gamma S stimulation, (ii) increased the sensitivity of phospholipase C to GTP and to GTP gamma S, and (iii) did not modify the stimulation of phospholipase C induced by maximal doses of GTP gamma S. Unlike sodium fluoride, GTP gamma S elicited an irreversible activation of phospholipase C. Calcium, GTP gamma S and sodium fluoride stimulated the phospholipase C activity via mechanisms sharing a common step, since their maximal effects were not additive. Cholera toxin treatment, known to produce complete ADP-ribosylation of 'alpha s' subunits, partially reduced the basal and the maximal GTP gamma S-mediated stimulation of phospholipase C activity as well as that caused by vasopressin. This inhibition was not mimicked by treatment with either forskolin or pertussis toxin.

Adenosine Diphosphate Ribose↗
PubMed1989

Lymphoepithelioma-like carcinoma of the lung.

Originally described in the nasopharynx, lymphoepitheliomas are undifferentiated carcinomas with prominent lymphoid infiltration. Recently this tumor has been described in a number of other sites. An association with prior infection by the Epstein-Barr virus has been recognized in cases from the nasopharynx. We report four cases of lymphoepithelioma-like carcinoma arising in the lung. Epstein-Barr virus serology indicated prior infection in two cases, one of which was also found by in situ hybridization to have the virus genome. Lymphoepithelioma-like carcinoma must be considered in the differential diagnosis of primary lung tumors, particularly when an extensive infiltrate by lymphoid tissue is present and may even suggest lymphoma.

Aged↗
PubMed1989

[Chronic diarrhea with hypergastrinemia and achlorhydria without gastritis in a 5-year-old child].

We report a case of chronic diarrhea due to hypergastrinemia with achlorhydria but without gastritis in a five-year-old boy. Symptoms responded promptly to oral administration of hydrochloric acid and resolved completely after one year of treatment. The pathophysiologic situation in this patient closely resembled that normally seen in neonates, suggesting prolonged but nevertheless transient immaturity of gastric secretions.

Achlorhydria↗
PubMed1989

Effect of N2O on segmental left ventricular function and effective arterial elastance in pigs when added to a halothane-fentanyl-pancuronium anesthetic technique.

The interaction of various concentrations of N2O and a stable halothane-fentanyl-pancuronium anesthetic technique was examined in nine pigs. Segmental myocardial contractility was measured with the end-systolic pressure-length relationship (Ees), and the effective arterial elastance (Ea) was quantified based on the Windkessel model. The addition of 30, 50, and 70% N2O did not change myocardial contractility or the effective arterial elastance. During the 30 and 70% N2O challenge, however, arterial capacitance decreased significantly from a mean (+/- SEM) 0.86 +/- 0.15 to 0.71 +/- 0.0.11 mL/mm Hg with 30% N2O (P less than 0.05) and from 0.90 +/- 0.09 to 0.71 +/- 0.07 mL/mm Hg (P less than 0.05) with 70% N2O. A dose-response relationship for the effect on the arterial capacitance could not be demonstrated. We concluded that in the presence of halothane, fentanyl, and pancuronium, N2O does not depress the normal myocardium or change left ventricular afterload. The decrease in arterial capacitance that occurred when 30 and 70% N2O were given was not sufficient to change the effective afterload and appears to be of no importance to normal left ventricular function.

Animals↗
PubMed1989

Effect of various propofol plasma concentrations on regional myocardial contractility and left ventricular afterload.

The cardiovascular effects of propofol infusions, designed to maintain constant plasma concentrations, were examined in an open-chested pig model. Regional myocardial contractility was measured with the end-systolic pressure-length relationship (Ees) and left ventricular afterload quantified by the effective arterial elastance (Ea). The propofol plasma concentrations in this study varied between 0 and 7.73 (SEM 0.96) micrograms/mL. A significant correlation for the increasing propofol plasma concentration and a decrease in myocardial contractility (P = 0.0056) was demonstrated, and the Ea remained constant. This gave rise to a reduction in stroke volume (P = 0.002) and, combined with a decrease in the heart rate (P = 0.0001), led to a reduction in the cardiac output (P = 0.0001). When the propofol infusion was stopped, myocardial contractility did not recover in parallel with the decrease in plasma propofol concentration.

Anesthetics↗
PubMed1988

Cholera-toxin and corticotropin modulation of inositol phosphate accumulation induced by vasopressin and angiotensin II in rat glomerulosa cells.

Vasopressin (VP) and angiotensin II (AT II) stimulate the production of inositol phosphates (IP) in rat glomerulosa cells. Guanosine 5'-[gamma-thio]triphosphate (GTP[S]), but not VP or AT II, stimulates IP production in a myo-[3H]inositol-prelabelled glomerulosa-cell membrane preparation. In combination with GTP[S], these hormones potentiate the response to GTP[S], indicating the existence of a G-protein involved in the coupling of the VP and AT II receptor with the phospholipase C. ADP-ribosylation with pertussis toxin (IAP) revealed the specific labelling of a single molecule of 41 kDa. No significant inhibition of VP- or AT II-stimulated IP accumulation was detected in intact cells when the whole 41 kDa molecule was endogenously ADP-ribosylated by IAP treatment. On the contrary, when glomerulosa cells were infected with cholera toxin (CT), both the VP- and AT II-stimulated IP accumulations were inhibited in a dose-dependent manner. Yet these effects were partial even at high concentrations of CT, and could not be related to the ADP-ribosylation of 'alpha s' molecules. Similarly, when the cells were infected with 1 microgram of CT/ml, the specific binding of VP and AT II decreased by 50-60%. Such results may signify that the treatment primarily affects the densities of the hormone receptors. When glomerulosa cells were incubated for 15 h in the presence of 10 nM-corticotropin (ACTH), a condition in which the intracellular concentration of cyclic AMP was increased 3-fold, the maximum IP response to 0.1 microM-VP or -AT II was decreased by 50%. When similar experiments were carried out only after a 15 min incubation period with the same concentration of ACTH, the increase in cyclic AMP was more pronounced, but no inhibition of hormone-induced IP accumulation was observed. Altogether, these results may suggest that CT exerts its action on the VP- or AT II-sensitive phospholipase C systems via a prolonged increase in intracellular cyclic AMP.

Adenosine Diphosphate↗
PubMed1988

Diffuse arterial narrowing as a result of intimal proliferation: a delayed complication of embolectomy with the Fogarty balloon catheter.

Most complications of embolectomy with the Fogarty balloon catheter are recognized early and have received ample attention in the surgical and radiologic literature. However, the delayed complication of diffuse arterial narrowing causing severe ischemia has received little emphasis, perhaps because follow-up arteriography is not always performed. This report describes five patients--women 43 to 62 years of age--with progressive leg ischemia discovered 2 to 4 months after embolectomy with the balloon catheter. Angiography showed a characteristic pattern of severe, smooth narrowing of that portion of the artery in which balloon embolectomy was performed. Pathologic examination of arterial specimens, available in two of the five patients, revealed marked intimal cellular proliferation, which narrowed the arteries severely without evidence of thrombosis, significant atheromatosis, or active arteritis. The cause appears to be intimal damage by the balloon. Embolectomy with the balloon catheter should be done especially carefully in relatively young women.

Adult↗
PubMed1987

Vasopressin receptors from cultured mesangial cells resemble V1a type.

Mesangial cells respond to vasopressin by contraction and increased prostaglandin production. The purpose of the present study is to characterize vasopressin receptors from these cells. Glomeruli were isolated from rat kidneys and plated for explant growth of mesangial cells. Membranes were prepared from cells grown for 6 wk and tested for their ability to bind [3H]vasopressin (lysine vasopressin). These membranes contained a single class of specific vasopressin binding sites [equilibrium dissociation constant (Kd) = 10 +/- 1 nM, maximal binding capacity (Bmax) = 270 +/- 7 fmol/mg protein for 5 determinations]. Vasopressin induced a dose-dependent (apparent Kact value = 2 nM) accumulation of labeled inositol phosphates in myo[3H]inositol-prelabeled mesangial cells incubated in the presence of 10 mM of Li. Conversely, vasopressin failed to alter the adenylate cyclase activity of mesangial cell membranes. Competition experiments with a series of vasopressin structural analogues that have different degrees of affinity for V2-(renal), V1a- (vascular and hepatic), and V1b- (adenohypophyseal) receptors, indicated that vasopressin receptors from rat glomerular mesangial cells resemble the V1a- receptor subtype.

Animals↗
PubMed1987

Iodination of vasopressin analogues with agonistic and antagonistic properties: effects on biological properties and affinity for vascular and renal vasopressin receptors.

Twelve L- and D-tyrosine-containing vasopressin analogues were prepared in their mono- and diiodinated forms. These include six arginine vasopressin (AVP) vascular (V1) type antagonists/antidiuretic (V2) agonists, four V1/V2 antagonists, and two V1/V2 agonists, one of which is AVP itself. Ten peptides were iodinated on the tyrosyl residue in position 2; two were iodinated on a tyrosyl amide residue replacing the glycyl amide residue at position 9. All peptides were tested both for their biological activities in vivo (rat vasopressor and antidiuretic tests) and for their ability to bind to vasopressin receptors of the V1 (vascular) and V2 (renal) types from rat liver and rat kidney membranes, respectively. It is shown that monoiodination of the tyrosyl residue in the vasopressin analogues that were tested either preserves or reduces to a highly variable extent the in vivo and in vitro biological activities of these analogues. In most cases diiodonitation resulted in a marked decrease in biological activity. The effects of iodination on the affinity of vasopressin analogues for hepatic V1 receptors and renal V2 receptors were more related to the affinity of the noniodinated peptide for these receptors than to the biological properties (antagonist versus agonist) of the tested analogues, the nature (L versus D) of the iodinated tyrosyl residue, or the position (2 versus 9) at which this residue was introduced. The loss of affinity due to iodination was usually more pronounced for peptides exhibiting high affinity for vasopressin receptors. However, we show that among the monoiodinated peptides some (especially monoiodinated [2-D-Tyrosine]-AVP) retained enough affinity for vasopressin binding sites to suggest that their radioiodinated conterparts would be promising labeled ligands for use in studies in vasopressin receptors.

Animals↗
PubMed1987

Giant cell pneumonia caused by parainfluenza type 3 in a patient with acute myelomonocytic leukemia.

A 4 1/2-year-old boy with acute myelomonocytic leukemia developed fever, neutropenia, and a prolonged respiratory illness while receiving maintenance chemotherapy. An open lung biopsy specimen demonstrated a giant cell pneumonia with intracytoplasmic and probable intranuclear viral inclusions of the paramyxovirus type. Serologic studies demonstrated convincing evidence of a parainfluenza type 3 infection. Although parainfluenza type 3-induced giant cell pneumonia has been reported in infants with the severe combined immunodeficiency syndrome, to our knowledge, this is the first reported case of this complication in a patient with leukemia.

Child, Preschool↗
PubMed1986

Angiotensin II and dopamine modulate both cAMP and inositol phosphate productions in anterior pituitary cells. Involvement in prolactin secretion.

Despite their opposite effects on prolactin secretion, both dopamine and angiotensin II inhibit adenylate cyclase activity in homogenates of anterior pituitary cells in primary culture. Dopamine and angiotensin II inhibition of adenylate cyclase was not additive, suggesting that both neurohormones inhibit the adenylate cyclase of the lactotroph cells. Pretreatment with Bordetella pertussis toxin (islet activator protein) completely suppressed the dopamine-induced inhibition of both adenylate cyclase and prolactin secretion. The islet activator protein also reversed the angiotensin II-induced inhibition of the adenylate cyclase activity. In contrast, angiotensin II stimulation of prolactin release was not affected by the toxin. Angiotensin II also induced a dose-dependent stimulation of inositol phosphates (250%) with an EC50 of 0.1 nM, close to that observed for prolactin secretion. Islet activator protein pretreatment did not block the stimulation of inositol phosphate production. Dopamine inhibited the angiotensin II-stimulated prolactin release and the production of inositol phosphates induced by angiotensin II. It is concluded that angiotensin II and dopamine receptors of lactotroph cells are able to modulate both cAMP and inositol phosphate production. The dopamine receptor of lactotrophs appears to be the first example of a receptor which is negatively coupled to the production of inositol phosphates.

Adenosine Diphosphate Ribose↗
PubMed1986

Electrocardiographic and histologic abnormalities in canine ceroid-lipofuscinosis (CCL).

Electrocardiograms were recorded in a longitudinal study on six adult dogs with canine ceroid-lipofuscinosis (CCL) and compared with those of four unaffected animals. Two dogs exhibited minor conduction abnormalities, QRS-notching and LVH at 12 months of age. By 24 to 25 months of age, the underlying cardiac rhythm was that of a pronounced sinus arrhythmia. Some dogs developed premature atrial beats, A-V dissociation or tachycardia. No gross cardiac abnormalities were noted at necropsy, but histologically, autonomic ganglion cells in the atrium, near the conducting system and in ventricular myocardial cells were filled with autofluorescent lipopigments. Quantification by micro-spectrophotometry showed peak emission at 538 nm. At the ultrastructural level, these fluorescent particles consisted of collections of curvilinear and lamellar profiles, similar to those present in other viscera. Ceroid-lipofuscinosis has been utilized for many years as a model for human ceroid-lipofuscinosis and the results described here are similar to those previously reported in hearts of patients with this disease. Because related lipopigments accumulate in normal aging of the heart and contraction/conduction abnormalities develop with time, the canine model may also be useful in aging studies as well. The studies described here are the first to demonstrate possible structural-functional relationships in the heart of dogs with CCL.

Animals↗
PubMed1983

Histiocytosis X in the lung.

The histologic and clinical features of pulmonary histiocytosis X are discussed. The majority of patients are in the third and fourth decades of life. They present with nonspecific respiratory complaints and bilateral reticulonodular infiltrates that can be seen on chest radiographs. The histologic lesions of pulmonary histiocytosis X are scattered, discrete nodules that frequently center on small airways. The initially cellular nodules are replaced progressively by fibrous tissue. The cell infiltrates in active lesions contain variable numbers of eosinophils and histiocytes resembling Langerhans cells of the epidermis (Hx cells). In most patients the disease resolves or stabilizes, leaving few, if any, significant residues. A minority of patients develop progressive pulmonary disease that is ultimately fatal. The cause of pulmonary histiocytosis X is unknown, but two recent series suggest a relationship to cigarette smoking.

Adolescent↗