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Biomedical subjects

J C Baker

Publications and source records attributed to J C Baker.

At least 19 recordsLinked to original sources

Experimental inoculation of pregnant swine with type 1 bovine viral diarrhoea virus.

The ability of bovine viral diarrhoea virus type 1 (BVDV-1) to induce transplacental infection in pigs was evaluated. Control pigs (n = 4) were sham-inoculated while infected pigs (n = 4) were intranasally inoculated with BVDV-1 on day 65 of gestation. Blood samples were tested throughout the study for BVDV and antibody to BVDV. On day 110 of gestation, a Caesarean section was performed. Serum was obtained for virus isolation and antibody determination from all piglets, and all experimental animals were killed. Tissues were collected for virus isolation and histopathology. Bovine viral diarrhoea virus was isolated on days 5 and 7 after infection and seroconversion was demonstrated in all infected gilts; however, BVDV was only isolated from one fetus from an infected pig. Viraemia and seroconversion were demonstrated in the pregnant gilts; however, transplacental infection at day 65 of gestation in the pig was not consistently demonstrated.

Animals↗

Study of cattle persistently infected with bovine viral diarrhea virus that lack detectable virus in serum.

OBJECTIVE: To determine whether cattle persistently infected with bovine viral diarrhea virus (BVDV) that lack virus detectable in serum by use of the immunoperoxidase microtiter assay (IPMA) can transmit the virus to susceptible herdmates and determine prevalence of these cattle. DESIGN: Clinical trial and serologic survey. SAMPLE POPULATION: 2 cattle and 1,952 blood samples. PROCEDURE: A persistently infected cow in which virus could not be detected in serum was housed with a BVDV-seronegative steer. Blood and nasal swab specimens were tested via virus isolation and serum virus neutralization. Parallel WBC preparations and sera from blood samples of 1,952 adult cows were screened for BVDV by use of IPMA. RESULTS: The steer seroconverted to BVDV within 4 weeks of contact with the cow. Virus was detected in sera and WBC of 5 adult cows that were verified as persistently infected by retest 3 weeks later. Cattle persistently infected with BVDV in which virus could not be detected in both serum and WBC by use of IPMA were not found. CONCLUSION AND CLINICAL RELEVANCE: Cattle persistently infected with BVDV in which virus cannot be detected in serum by use of IPMA may serve as virus reservoirs for infecting susceptible cattle. Persistent infection was detected at a prevalence of 0.26%. Screening adult cattle by use of IPMA on serum samples appears to be a reliable means of detecting persistent infection with BVDV. Prevalence of cattle persistently infected with BVDV that have negative results of IPMA on serum is extremely low.

Animals↗

Reaction mechanism for mammalian pyruvate dehydrogenase using natural lipoyl domain substrates.

The pyruvate dehydrogenase (E1) component of the pyruvate dehydrogenase complex (PDC) catalyzes a two-step reaction. Recombinant production of substrate amounts of the lipoyl domains of the dihydrolipoyl transacetylase (E2) component of the mammalian PDC allowed kinetic characterization of the rapid physiological reaction catalyzed by E1. Using either the N-terminal (L1) or the internal (L2) lipoyl domain of E2 as a substrate, analyses of steady state kinetic data support a ping pong mechanism. Using standard E1 preparations, Michaelis constants (Km) were 52 +/- 14 microM for L1 and 24.8 +/- 3.8 microM for pyruvate and k(cat) was 26.3 s(-1). With less common, higher activity preparations of E1, the Km values were > or =160 microM for L1 and > or =35 microM for pyruvate and k(cat) was > or =70 s(-1). Similar results were found with the L2 domain. The best synthetic lipoylated-peptide (L2 residues 163-177) was a much poorer substrate (Km > or =15 mM, k(cat) approximately equals 5 s(-1); k(cat)/Km decreased >1,500-fold) than L1 or L2, but a far better substrate in the E1 reaction than free lipoamide (k(cat)/Km increased >500-fold). Each lipoate source was an effective substrate in the dihydrolipoyl dehydrogenase (E3) reaction, but E3 had a lower Km for the L2 domain than for lipoamide or the lipoylated peptides. In contrast to measurements with slow E1 model reactions that use artificial acceptors, we confirmed that the natural E1 reaction, using lipoyl domain acceptors, was completely inhibited (>99%) by phosphorylation of E1 and the phosphorylation strongly inhibited the reverse of the second step catalyzed by E1. The mechanisms by which phosphorylation interferes with E1 activity is interpreted based on accrued results and the location of phosphorylation sites mapped onto the 3-D structure of related alpha-keto acid dehydrogenases.

Acetylation↗

Distinct regulatory properties of pyruvate dehydrogenase kinase and phosphatase isoforms.

The mammalian pyruvate dehydrogenase complex (PDC) plays central and strategic roles in the control of the use of glucose-linked substrates as sources of oxidative energy or as precursors in the biosynthesis of fatty acids. The activity of this mitochondrial complex is regulated by the continuous operation of competing pyruvate dehydrogenase kinase (PDK) and pyruvate dehydrogenase phosphatase (PDP) reactions. The resulting interconversion cycle determines the fraction of active (nonphosphorylated) pyruvate dehydrogenase (E1) component. Tissue-specific and metabolic state-specific control is achieved by the selective expression and distinct regulatory properties of at least four PDK isozymes and two PDP isozymes. The PDK isoforms are members of a family of serine kinases that are not structurally related to cytoplasmic Ser/Thr/Tyr kinases. The catalytic subunits of the PDP isoforms are Mg2+-dependent members of the phosphatase 2C family that has binuclear metal-binding sites within the active site. The dihydrolipoyl acetyltransferase (E2) and the dihydrolipoyl dehydrogenase-binding protein (E3BP) are multidomain proteins that form the oligomeric core of the complex. One or more of their three lipoyl domains (two in E2) selectively bind each PDK and PDP1. These adaptive interactions predominantly influence the catalytic efficiencies and effector control of these regulatory enzymes. When fatty acids are the preferred source of acetyl-CoA and NADH, feedback inactivation of PDC is accomplished by the activity of certain kinase isoforms being stimulated upon preferentially binding a lipoyl domain containing a reductively acetylated lipoyl group. PDC activity is increased in Ca2+-sensitive tissues by elevating PDP1 activity via the Ca2+-dependent binding of PDP1 to a lipoyl domain of E2. During starvation, the irrecoverable loss of glucose carbons is restricted by minimizing PDC activity due to high kinase activity that results from the overexpression of specific kinase isoforms. Overexpression of the same PDK isoforms deleteriously hinders glucose consumption in unregulated diabetes.

Amino Acid Sequence↗

Relationship between degree of viremia and disease manifestation in calves with experimentally induced bovine viral diarrhea virus infection.

OBJECTIVE: To compare degree of viremia and disease manifestations in calves with type-I and -II bovine viral diarrhea virus (BVDV) infection. ANIMALS: 16 calves. PROCEDURE: Colostrum-deprived calves obtained immediately after birth were assigned to 1 control and 3 treatment groups (4 calves/group). Calves in treatment groups were inoculated (day 0) by intranasal instillation of 10(7) median tissue culture infective dose BVDV 890 (type II), BVDV 7937 (type II), or BVDV TGAN (type I). Blood cell counts and virus isolation from serum and leukocytes were performed daily, whereas degree of viremia was determined immediately before and 4, 6, 8, and 12 days after inoculation. Calves were euthanatized on day 12, and pathologic, virologic, and immunohistochemical examinations were performed. RESULTS: Type-II BVDV 890 induced the highest degree of viremia, and type-I BVDV TGAN induced the lowest. Virus was isolated more frequently and for a longer duration in calves inoculated with BVDV 890. A parallel relationship between degree of viremia and rectal temperature and an inverse relationship between degree of viremia and blood cell counts was observed. Pathologic and immunohistochemical examinations revealed more pronounced lesions and more extensive distribution of viral antigen in calves inoculated with type-II BVDV. CONCLUSIONS AND CLINICAL RELEVANCE: Degree of viremia induced during BVDV infection is associated with severity of clinical disease. Isolates of BVDV that induce a high degree of viremia may be more capable of inducing clinical signs of disease. Strategies (eg, vaccination) that reduce viremia may control clinical signs of acute infection with BVDV.

Animals↗

Platelet aggregation responses and virus isolation from platelets in calves experimentally infected with type I or type II bovine viral diarrhea virus.

Altered platelet function has been reported in calves experimentally infected with type II bovine viral diarrhea virus (BVDV). The purpose of the present study was to further evaluate the ability of BVDV isolates to alter platelet function and to examine for the presence of a virus-platelet interaction during BVDV infection. Colostrum-deprived Holstein calves were obtained immediately after birth, housed in isolation, and assigned to 1 of 4 groups (1 control and 3 treatment groups). Control calves (n = 4) were sham inoculated, while calves in the infected groups (n = 4 for each group) were inoculated by intranasal instillation with 10(7) TCID50 of either BVDV 890 (type II), BVDV 7937 (type II), or BVDV TGAN (type I). Whole blood was collected prior to inoculation (day 0) and on days 4, 6, 8, 10, and 12 after inoculation for platelet function testing by optical aggregometry by using adenosine diphosphate and platelet activating factor. The maximum percentage aggregation and the slope of the aggregation curve decreased over time in BVDV-infected calves; however, statistically significant differences (Freidman repeated measures ANOVA on ranks, P < 0.05) were only observed in calves infected with the type II BVDV isolates. Bovine viral diarrhea virus was not isolated from control calves, but was isolated from all calves infected with both type II BVDV isolates from days 4 through 12 after inoculation. In calves infected with type I BVDV, virus was isolated from 1 of 4 calves on days 4 and 12 after inoculation and from all calves on days 6 and 8 after inoculation. Altered platelet function was observed in calves infected with both type II BVDV isolates, but was not observed in calves infected with type I BVDV. Altered platelet function may be important as a difference in virulence between type I and type II BVDV infection.

Adenosine Diphosphate↗

Marked differences between two isoforms of human pyruvate dehydrogenase kinase.

Pyruvate dehydrogenase kinase (PDK) isoforms 2 and 3 were produced via co-expression with the chaperonins GroEL and GroES and purified with high specific activities in affinity tag-free forms. By using human components, we have evaluated how binding to the lipoyl domains of the dihydrolipoyl acetyltransferase (E2) produces the predominant changes in the rates of phosphorylation of the pyruvate dehydrogenase (E1) component by PDK2 and PDK3. E2 assembles as a 60-mer via its C-terminal domain and has mobile connections to an E1-binding domain and then two lipoyl domains, L2 and L1 at the N terminus. PDK3 was activated 17-fold by E2; the majority of this activation was facilitated by the free L2 domain (half-maximal activation at 3.3 microm L2). The direct activation of PDK3 by the L2 domain resulted in a 12.8-fold increase in k(cat) along with about a 2-fold decrease in the K(m) of PDK3 for E1. PDK3 was poorly inhibited by pyruvate or dichloroacetate (DCA). PDK3 activity was stimulated upon reductive acetylation of L1 and L2 when full activation of PDK3 by E2 was avoided (e.g. using free lipoyl domains or ADP-inhibited E2-activated PDK3). In marked contrast, PDK2 was not responsive to free lipoyl domains, but the E2-60-mer enhanced PDK2 activity by 10-fold. E2 activation of PDK2 resulted in a greatly enhanced sensitivity to inhibition by pyruvate or DCA; pyruvate was effective at significantly lower levels than DCA. E2-activated PDK2 activity was stimulated >/=3-fold by reductive acetylation of E2; stimulated PDK2 retained high sensitivity to inhibition by ADP and DCA. Thus, PDK3 is directly activated by the L2 domain, and fully activated PDK3 is relatively insensitive to feed-forward (pyruvate) and feed-back (acetylating) effectors. PDK2 was activated only by assembled E2, and this activated state beget high responsiveness to those effectors.

Acetyl Coenzyme A↗

Development of a standardized methodology for double-blind, placebo-controlled food challenge in patients with brittle asthma and perceived food intolerance.

OBJECTIVE: To develop a standardized, double-blind, placebo-controlled, food challenge (DBPCFC) methodology for identifying food intolerance in patients with brittle asthma. SUBJECTS/SETTING: Patients with brittle asthma and perceived food intolerance were studied in hospital. DESIGN: Each of 3 protocols began with 5 days of dietary exclusion. Protocol 1 consisted of open food challenges in 29 patients, protocol 2 consisted of 2 daily DBPCFCs in 22 patients, and protocol 3 involved 1 daily DBPCFC in 18 patients. Total immunoglobulin E level was measured and food-specific radioallergosorbent tests and skin prick tests were conducted. A standard panel of hyperallergenic foods were masked in a soup (developed specially for this study) for every food challenge. Peak expiratory flow, forced expiratory volume, and symptoms were assessed as objective measures of response. Open food challenges at home followed each protocol. Each protocol took approximately 14 days in the hospital and 4 to 6 months at home. RESULTS: For protocols 1, 2 and 3, positive reactions were experienced by 52%, 55%, and 66% of patients, respectively. Radioallergosorbent tests and skin prick tests were shown to have 40% and 71% sensitivity, respectively, and 74% and 77% specificity for predicting a positive food challenge. APPLICATIONS/CONCLUSIONS: The high prevalence of food intolerance in patients with brittle asthma was confirmed, as was the poor positive predictive value of skin prick tests and radioallergosorbent tests. The food challenge method developed enables standardized identification of food intolerances in patients with brittle asthma and may be useful in other groups.

Adult↗

Regression of poloxamer 407-induced atherosclerotic lesions in C57BL/6 mice using atorvastatin.

HMG-CoA reductase inhibitor drugs or 'statins' have been shown to effectively reduce plasma total cholesterol (CHOL), CHOL associated with low-density-lipoprotein (LDL), and triglycerides (TG). In addition, slight elevations in HDL-CHOL are also typically observed. Poloxamer 407 (P-407), a nonionic surfactant, effectively elevates both plasma CHOL and especially TG in a dose-controlled fashion and results in formation of atherosclerotic lesions in the aortas of C57BL/6 mice without the requirement of dietary cholic acid [1,2]. The purpose of the present study was to assess whether a typical statin, namely atorvastatin (Lipitor(R)) would significantly reduce P-407-induced hypercholesterolemia and hypertriglyceridemia as well as cause regression of atherosclerotic lesions resulting from administration of P-407 to C57BL/6 mice. C57BL/6 mice in the present study were treated with either normal saline (C, controls), 0.5 g/kg of P-407 (P), or a high-fat, high-cholesterol, cholate-containing diet (HF) for 120 days. Mice in all groups were then equally and randomly divided and treated with either atorvastatin or saline for an additional 120 days. Beginning at Day 121 and using mice in groups P and HF as an example, one-fourth of the mice in each group received 20 mg/kg per day of atorvastatin with either concomitant HF feeding or P-407 administration ('progression' treatment groups), one-fourth received 20 mg/kg per day of atorvastatin following cessation of HF feeding or P-407 administration, one-fourth received saline (placebo) with either simultaneous HF feeding or P-407 administration ('progression' placebo groups), and one-fourth received saline (placebo) following cessation of HF feeding or P-407 administration. Total plasma CHOL was significantly (P<0.01) lower for mice in groups P and HF when administered atorvastatin relative to saline, but remained significantly (P<0.05) elevated compared to total plasma CHOL of C mice. With discontinuation of either P-407 administration or HF feeding, total plasma CHOL declined rapidly in both P and HF mice with atorvastatin-treated mice generally demonstrating lower plasma CHOL concentrations relative to saline-treated mice. Total plasma TG was significantly (P<0.01) lower for mice in group P administered atorvastatin relative to saline, but remained significantly (P<0.05) elevated compared to plasma TG of C mice. With discontinuation of P-407 administration, total plasma TG declined rapidly in P mice with atorvastatin-treated mice typically demonstrating lower plasma TG concentrations relative to saline-treated P mice. Aortas of mice treated with 20 mg/kg per day of atorvastatin in both groups P and HF, whether maintained on the HF-diet or treated with P-407 from Day 120 to 240 or whether each treatment was terminated at Day 120, revealed no presence of atherosclerotic lesions relative to saline-treated mice and were indistinguishable from aortas retrieved from C mice. Atorvastatin at a dose of 20 mg/kg per day not only significantly reduced the plasma CHOL and TG concentrations, but also resulted in regression of atherosclerotic lesions induced in C57BL/6 mice by administration of P-407 or ingestion of a HF-diet containing cholic acid.

Analysis of Variance↗

Diet and asthma.

The role of food intolerance in asthma is well recognized, and where food avoidance measures are instituted considerable improvement in asthma symptoms and in reduction in drug therapy and hospital admissions can result. These benefits may have a greater impact in those patients with greater symptoms. However, the promise of such benefits should not result in an approach which ignores inhaled drug therapy, or in a dietary regime which is inappropriate in the face of mild symptoms. Whilst sub-optimal intake of dietary nutrients is also a recently recognized potential risk factor for asthma, available data are insufficient to implicate any as casual. A number of studies have sought to establish the role of the antioxidant vitamins, A, C and E and selenium, yet others of the elements sodium and magnesium. Sub-optimal nutrient intake may enhance asthmatic inflammation, consequently contributing to bronchial hyperreactivity. Prospective studies of supplementation therapy are needed to confirm this.

Antioxidants↗

Serotyping of Mannheimia (Pasteurella) haemolytica isolates from the upper Midwest United States.

Mannheimia (Pasteurella) haemolytica biotype A serotype1 (A1) is the primary bacterial agent responsible for the clinical signs and pathophysiologic events in bovine pneumonic pasteurellosis. The goal of this study was to determine the prevalence of other serotypes of M. haemolytica biotype A organisms obtained from the upper Midwest diagnostic laboratories. A total of 147 M. haemolytica isolates were collected from Minnesota, South Dakota, and Michigan. Isolates were tested against M. haemolytica antisera obtained from the National Animal Disease Center, Ames, Iowa. Results indicated that M. haemolytica serotype 1 represented approximately 60%, serotype 6 represented 26%, and serotype 2 represented 7% of the total examined isolates. In addition, 7% of the isolates were serotype 9, 11, or untypable. This finding suggests that M. haemolytica serotypes other than serotype 1 can be isolated from the lung lesions of diseased cattle and seem to be capable of causing the pathologic changes observed in the lung with pneumonic pasteurellosis.

Animals↗

Caprine mucopolysaccharidosis IIID: a preliminary trial of enzyme replacement therapy.

Mucopolysaccharidosis type IIID (MPS IIID) is a lysosomal storage disorder resulting from lack of activity of the lysosomal hydrolase N-acetylglucosamine 6-sulfatase (6S) (EC 3.1.6.14). The syndrome is associated with systemic and central nervous system (CNS) heparan sulfate glycosaminoglycan (HS-GAG) accumulation, secondary storage of lipids, and severe, progressive dementia. In this investigation, caprine MPS IIID, established as a large animal model for the human disease, was used to evaluate the efficacy of enzyme replacement therapy (ERT). Recombinant caprine 6S (rc6S) (1 mg/kg/dose) was administered intravenously to one MPS IIID goat kid at 2, 3, and 4 wks of age. Five days after the last dose, the uronic acid (UA) content and the composition of uncatabolized HS-GAG fractions in the brain of the ERT-treated MPS IIID kid were similar to those from a control, untreated MPS IIID animal. However, hepatic uronic acid levels in the treated MPS IIID kid were approximately 90% lower than those in the untreated MPS IIID control; whereas the composition of the residual hepatic HS-GAG was identical to that in the untreated animal. Marked reduction of lysosomal storage vacuoles in hepatic cells of the treated MPS IIID kid was observed, but ERT had no effect on CNS lesions. No residual 6S activity was detected in brain or liver. This preliminary investigation indicates that other treatment regimens will be necessary to ameliorate MPS III-related CNS lesions.

Animals↗

Wnt signaling in Xenopus embryos inhibits bmp4 expression and activates neural development.

We report a new role for Wnt signaling in the vertebrate embryo: the induction of neural tissue from ectoderm. Early expression of mouse wnt8, Xwnt8, beta-catenin, or dominant-negative GSK3 induces the expression of neural-specific markers and inhibits the expression of Bmp4 in Xenopus ectoderm. We show that Wnt8, but not the BMP antagonist Noggin, can inhibit Bmp4 expression at early gastrula stages. Furthermore, inhibition of beta-catenin activity in the neural ectoderm of whole embryos by a truncated TCF results in a decrease in neural development. Therefore, we suggest that a cleavage-stage Wnt signal normally contributes to an early repression of Bmp4 on the dorsal side of the embryo and sensitizes the ectoderm to respond to neural inducing signals from the organizer. The Wnt targets Xnr3 and siamois have been shown previously to have neuralizing activity when overexpressed. However, antagonists of Wnt signaling, dnXwnt8 and Nxfrz8, inhibit Wnt-mediated Xnr3 and siamois induction, but not neural induction, suggesting an alternative mechanism for Bmp repression and neuralization. Conversely, dnTCF blocks both Wnt-mediated Xnr3 and neural induction, suggesting that both pathways require this transcription factor.

Animals↗

Drosophila dSmad2 and Atr-I transmit activin/TGFbeta signals.

BACKGROUND: Much is known about the three subfamilies of the TGFbeta superfamily in vertebrates-the TGFbetas, dpp/BMPs, and activins. Signalling in each subfamily is dependent on both shared and unique cell surface receptors and Smads. In invertebrates, mutants for BMP pathway components have been extensively characterized, but thus far, evidence for an activin- or TGFbeta-like pathway has been lacking, preventing the use of the extensive genetic tools available for studying several key issues of TGFbeta signalling. RESULTS: Here we report the identification of dSmad2, a new Drosophila Smad which is most related to the activin/TGFbeta-pathway Smads, Smad2 and Smad3. We show that dSmad2 induces activin responsive genes in Xenopus animal cap assays. dSMAD2 is phosphorylated by ATR-I and PUNT, but not by activated THICK VEINS, and translocates to the nucleus upon activation. Furthermore, we show that dSMAD2 complexes with MEDEA only in the presence of ATR-I and PUNT. dSmad2 is expressed in the imaginal disks and in the outer proliferation centre of the larval brain, suggesting that it may have important proliferative and patterning roles during Drosophila development. CONCLUSION: Our data provide evidence for the existence of an activin/TGFbeta pathway in Drosophila. We show that dSmad2 participates in this pathway, and that it functions with Atr-I and punt. We show that Medea also participates in this pathway, indicating the conservation of roles for Co-Smads in diverse phyla. Expression patterns of dSmad2 suggest that it functions in imaginal disks and in the brain, in tissues that undergo extensive patterning and proliferation.

Activin Receptors↗

Potential downregulation of HMG-CoA reductase after prolonged administration of P-407 in C57BL/6 mice.

This study investigated the potential alteration in the amount of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase messenger RNA (mRNA) and lipoprotein lipase (LPL) mRNA in the livers of C57BL/6 mice after long-term (200 days) treatment with the nonionic surfactant called poloxamer 407 (P-407). Previously, P-407 has been used to produce a dose-controlled hyperlipidemic state in C57BL/6 mice with subsequent formation of atherosclerotic lesions. Five groups of mice were studied; controls (C); mice fed a standard chow diet enriched with only cholic acid (CH); mice fed the high-cholesterol, high-fat Paigen diet (HF); mice treated with 0.5 g/kg P-407 every third day (P); and mice administered 0.5 g/kg P-407 every third day while consuming a diet identical to that of mice in group CH (PC). Neither a significant (p < 0.05) weight loss nor alteration in liver enzymes (AST and ALT) were observed for any group throughout the study when compared with the control mice. Total plasma cholesterol (CHOL) was significantly elevated compared with controls for mice in groups HF, P, and PC, whereas total plasma triglycerides (TG) were significantly increased for mice in only groups P and PC. Long-term ingestion of a high-fat diet or a diet enriched in cholic acid resulted in a significant (p < 0.05) reduction in HDL-CHOL when compared with controls. Plasma samples assayed at 200 days for mice in groups HF and P showed a shift in the lipoprotein fraction distribution primarily to VLDL-CHOL as compared with mice in group C in which, as expected, most of the CHOL was contained in the HDL fraction. The biologic activity of HMG-CoA reductase assayed in hepatic microsomal homogenates was significantly reduced for mice in groups CH (p < 0.01), HF (p < 0.01), and PC (p < 0.05), but not for mice in group P, when compared with control. A statistical analysis of the data demonstrated significant (p < 0.05) reductions in the HMG-CoA reductase mRNA levels in hepatic tissue for all treatment groups relative to mRNA levels determined for mice in group C. In contrast, no treatment group demonstrated a significant difference in hepatic LPL mRNA levels when compared with mRNA levels determined for control animals. These data demonstrate that P-407 administration to C57BL/6 mice significantly decreased the amount of HMG-CoA reductase mRNA detected in liver.

Animals↗

Dietary antioxidants and magnesium in type 1 brittle asthma: a case control study.

BACKGROUND: Type 1 brittle asthma is a rare form of asthma. Atopy, psychosocial factors and diet may contribute to this condition. As increased dietary magnesium has a beneficial effect on lung function and selenium, vitamins A, C and E have antioxidant properties, a study was undertaken to test the hypothesis that patients with brittle asthma have diets deficient in these nutrients compared with subjects with non-brittle asthma and healthy adults. METHODS: A case control study of the dietary intakes of 20 subjects with brittle asthma, 20 with non-brittle asthma, and 20 healthy adults was performed using five day weighed dietary records. Intake of magnesium was the primary outcome measure with selenium and vitamins A, C and E as secondary outcomes. Serum levels were measured at the same time as the dietary assessment. RESULTS: Sixty subjects (27 men) of mean age 49.5 years were recruited and completed the study. Subjects with brittle asthma had statistically lower median dietary intakes of vitamins A and E than the other groups (vitamin A: brittle asthma 522.5 micrograms/day, non-brittle asthma 869.5 micrograms/day, healthy adults 806.5 micrograms/day; vitamin E: brittle asthma 4.3 mg/day, non-brittle asthma 4.6 mg/day, healthy adults 4.5 mg/day). Median dietary intakes for the other nutrients were not significantly different between groups. Serum levels were within normal ranges for each nutrient in all subjects. Intakes less than the reference nutrient intake (RNI) for magnesium and vitamins A and C, and less than the safe intake (SI) for vitamin E were more likely in patients with brittle asthma than in those with non-brittle asthma. CONCLUSION: Nutrient deficiency and reduced antioxidant activity may contribute to disease activity in type 1 brittle asthma, although a prospective study of replacement therapy will be needed to confirm this hypothesis.

Ascorbic Acid Deficiency↗

Analysis of ruminant respiratory syncytial virus isolates by RNAse protection of the G glycoprotein transcripts.

Two different respiratory syncytial virus (RSV) radiolabeled probes were used to characterize the genetic heterogeneity of 25 ruminant RSV isolates by the ribonuclease protection assay. A 32P-radiolabeled antisense RNA probe was transcribed from cloned ovine and bovine RSV G glycoprotein genes and then hybridized with total RNA isolated from infected cells with various ruminant RSV isolates. The results of this study, along with previously published nucleotide sequence data of the ovine RSV G glycoprotein gene, suggest the presence of at least 2 ruminant RSV subgroups. One subgroup is represented by RSV isolated from respiratory disease outbreaks from calves and goats, and the other is represented by RSV isolated from sheep.

Animals↗

Experimental model of type II bovine viral diarrhea virus-induced thrombocytopenia in neonatal calves.

Thrombocytopenia has been associated with type II bovine viral diarrhea virus (BVDV) infection in immunocompetent cattle, but the mechanism is unknown. The purpose of the present study was to develop and characterize a model of type II BVDV-induced thrombocytopenia. Colostrum-deprived Holstein calves were obtained immediately after birth, given a BVDV-negative and BVDV antibody-negative plasma transfusion, housed in an isolation facility, and randomly assigned to either control (n = 4) or infected (n = 5) groups. Infected calves were inoculated by intranasal instillation on day 3 of age with 10(7) TCID50 of the prototype type II isolate, BVDV 890, whereas control calves were sham inoculated. Blood counts and virus isolations from serum, white blood cells, and platelets were performed daily until day 12 after infection, at which time all experimental calves were euthanatized, and pathologic, virologic, and immunohistochemical examinations were performed. On physical examination, the control calves remained normal, but the infected calves developed pyrexia and diarrhea characteristic of type II BVDV infection. The platelet count decreased in all infected calves, and a statistically significant difference in the platelet count between control and infected calves was observed on days 7-12 after infection. In addition, the mean platelet volume and white blood cell counts also decreased. Examination of the bone marrow from the infected calves revealed immunohistochemical staining for BVDV antigen in megakaryocytes and evidence of concurrent megakaryocyte necrosis and hyperplasia.

Animals↗