Iatrogenic actinomycetoma of neck and back successfully treated with sulphonamides.
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Adult↗
Biomedical subjects
S Dayal
Publications and source records attributed to S Dayal.
The determination of nicotinic acid in plasma by mixed-mode liquid chromatography-tandem mass spectrometry following ion exchange solid phase extraction.
An assay for nicotinic acid in plasma samples has been developed using ion exchange solid phase extraction in 96-well format followed by mixed-mode ion exchange/reversed-phase liquid chromatography with positive ion tandem mass spectrometry detection. The assay avoids the need for time-consuming derivatisation procedures or involatile ion-pair chromatography reagents. The assay is linear over the wide range 0.05-20 microg/mL, based on a 100 microL sample (correlation coefficient>0.99). The assay is accurate and precise (bias and coefficient of variation<18%) over this calibration range.
Administration, Oral↗
Genetic polymorphism of alpha-lactalbumin gene in riverine buffalo.
Alpha-lactalbumin (alpha-LA) is a major whey protein found in milk. Polymorphs of alpha-LA gene are reported to be significantly associated with milk production and constituent traits. Therefore, the present study was undertaken to detect polymorphism in alpha-LA at the genic level and to explore allelic variability at this locus. A total of 196 animals, belonging to four breeds of riverine buffalo viz. Bhadwari, Mehsana, Surti and Murrah were included under the present investigation. Two fragments i.e. 133 bp (Exon 1) and 159 bp (Exon 2) of alpha-LA gene were amplified by polymerase chain reaction and subsequently, single strand confirmation polymorphism (SSCP) study was carried out to identify different allelic pattern and genotypes of the animal included in the study. Both fragment of alpha-LA gene was found to be polymorphic in all the four breeds of riverine buffalo. Number of genotypes and allele varied breed to breed for both the fragments. In case of 133 bp fragment, four alleles A, B, C and D were found among different breeds of buffalo whereas in 159 bp fragment, five alleles namely A, B, C, D and E was found in different breeds. Nucleotide sequence data of different alleles showed the presence of both silent as well as functional mutation leading to variability in polypeptide chain.
Alleles↗
An efficient protocol for shoot regeneration and genetic transformation of pigeonpea [ Cajanus cajan (L) Millsp] using leaf explants.
A protocol for efficient plant regeneration from leaf explants of pigeonpea [ Cajanus cajan (L.) Millsp.] was developed for the production of transgenic plants. Leaf explants from 4- to 5-day-old in vitro raised seedlings were most efficient in producing multiple adventitious shoots in 90% of the explants on shoot induction medium [Murashige and Skoog (MS) medium +5.0 microM benzyladenine +5.0 microM kinetin]. Shoot buds originated from the petiolar cut end of the explants and elongated rapidly on medium containing 0.58 microM gibberellic acid. Over 80% of the elongated shoots rooted well on MS medium containing 11.42 microM indole-3-acetic acid and were transplanted with 100% success. The procedure reported here is very simple, efficient and reproducible, and is applicable across diverse genotypes of pigeonpea. The usefulness of this system for further studies on the genetic transformation of pigeonpea has been demonstrated in biolistics-mediated gene transfer by using nptII and uidA as marker genes, where 50% of the selected plants showed gene integration and expression.
Cajanus↗
Endothelial dysfunction and elevation of S-adenosylhomocysteine in cystathionine beta-synthase-deficient mice.
Hyperhomocysteinemia is associated with increased risk for cardiovascular events, but it is not certain whether it is a mediator of vascular dysfunction or a marker for another risk factor. Homocysteine levels are regulated by folate bioavailability and also by the methyl donor S-adenosylmethionine (SAM) and its metabolite S-adenosylhomocysteine (SAH). We tested the hypotheses that endothelial dysfunction occurs in hyperhomocysteinemic mice in the absence of folate deficiency and that levels of SAM and SAH are altered in mice with dysfunction. Heterozygous cystathionine beta-synthase-deficient (CBS(+/-)) and wild-type (CBS(+/+)) mice were fed a folate-replete, methionine-enriched diet. Plasma levels of total homocysteine were elevated in CBS(+/-) mice compared with CBS(+/+) mice after 7 weeks (27.1+/-5.2 versus 8.8+/-1.1 micromol/L; P<0.001) and 15 weeks (23.9+/-3.0 versus 13.0+/-2.3 micromol/L; P<0.01). After 15 weeks, but not 7 weeks, relaxation of aortic rings to acetylcholine was selectively impaired by 35% (P<0.05) and thrombomodulin anticoagulant activity was decreased by 20% (P<0.05) in CBS(+/-) mice. Plasma levels of folate did not differ between groups. Levels of SAH were elevated approximately 2-fold in liver and brain of CBS(+/-) mice, and correlations were observed between plasma total homocysteine and SAH in liver (r=0.54; P<0.001) and brain (r=0.67; P<0.001). These results indicate that endothelial dysfunction occurs in hyperhomocysteinemic mice even in the absence of folate deficiency. Endothelial dysfunction in CBS(+/-) mice was associated with increased tissue levels of SAH, which suggests that altered SAM-dependent methylation may contribute to vascular dysfunction in hyperhomocysteinemia.
Animals↗
Homocysteine-induced endoplasmic reticulum stress causes dysregulation of the cholesterol and triglyceride biosynthetic pathways.
Hepatic steatosis is common in patients having severe hyperhomocysteinemia due to deficiency for cystathionine beta-synthase. However, the mechanism by which homocysteine promotes the development and progression of hepatic steatosis is unknown. We report here that homocysteine-induced endoplasmic reticulum (ER) stress activates both the unfolded protein response and the sterol regulatory element-binding proteins (SREBPs) in cultured human hepatocytes as well as vascular endothelial and aortic smooth muscle cells. Activation of the SREBPs is associated with increased expression of genes responsible for cholesterol/triglyceride biosynthesis and uptake and with intracellular accumulation of cholesterol. Homocysteine-induced gene expression was inhibited by overexpression of the ER chaperone, GRP78/BiP, thus demonstrating a direct role of ER stress in the activation of cholesterol/triglyceride biosynthesis. Consistent with these in vitro findings, cholesterol and triglycerides were significantly elevated in the livers, but not plasmas, of mice having diet-induced hyperhomocysteinemia. This effect was not due to impaired hepatic export of lipids because secretion of VLDL-triglyceride was increased in hyperhomocysteinemic mice. These findings suggest a mechanism by which homocysteine-induced ER stress causes dysregulation of the endogenous sterol response pathway, leading to increased hepatic biosynthesis and uptake of cholesterol and triglycerides. Furthermore, this mechanism likely explains the development and progression of hepatic steatosis and possibly atherosclerotic lesions observed in hyperhomocysteinemia.
Animals↗
Cloning, expression, and chromosome mapping of the murine Hip/Rpl29 gene.
We previously have identified murine heparin/heparan sulfate-interacting protein (HIP) identical to mouse ribosomal protein L29 that is, like its human orthologue, distinctively expressed both on the cell surface and intracellularly in different adult tissues and cell types. In the present study, we show that mouse HIP/RPL29 is encoded by a single mRNA and that it is expressed to different extents in most of the tissues of the developing embryo without restriction to a specific cell type. We isolated the single-copy gene coding for murine Hip/Rpl29 among a large number of pseudogenes, established its structure, and assigned its location to distal chromosome 9. Similar to other ribosomal protein promoters, the promoter of Hip/Rpl29 is rich in polypyrimidine tracts, contains binding motifs for ubiquitously expressed transcription factors, and lacks a TATA box. Progressive 5' deletion analyses identified a strong enhancer region that includes CT-rich sequences and a potential consensus binding site for NF-kappaB. These data will provide valuable tools to progress the understanding of HIP/RPL29 function as a ribosomal protein and/or as a regulator of growth and cell adhesion through interaction with heparan sulfate proteoglycans.
Animals↗
Involvement of Tcf/Lef in establishing cell types along the animal-vegetal axis of sea urchins.
Members of the Tcf/Lef family interact with beta-catenin to activate programs of gene expression during development. Recently beta-catenin was shown to be essential for establishing cell fate along the animal-vegetal axis of the sea urchin embryo. To examine the role of Tcf/Lef in sea urchins we cloned a Strongylocentrotus purpuratus Tcf/Lef homolog. Expression of SpTcf/Lef was maximal when beta-catenin became localized to nuclei of vegetal blastomeres, consistent with its acting in combination with beta-catenin to specify vegetal cell fates. Expression of a dominant-negative SpTcf/Lef inhibited primary and secondary mesenchyma, endoderm, and aboral ectoderm formation in a manner similar to that observed when nuclear accumulation of beta-catenin was prevented. Our results suggest that SpTcf/Lef functions by interacting with beta-catenin to specify cell fates along the sea urchin animal-vegetal axis.
Amino Acid Sequence↗
Folate dependence of hyperhomocysteinemia and vascular dysfunction in cystathionine beta-synthase-deficient mice.
Hyperhomocysteinemia is a risk factor for stroke, myocardial infarction, and venous thrombosis. Moderate hyperhomocysteinemia is associated with impaired endothelial function, but the mechanisms responsible for endothelial dysfunction in hyperhomocysteinemia are poorly understood. We have used genetic and dietary approaches to produce hyperhomocysteinemia in mice. Heterozygous cystathionine beta-synthase-deficient mice (CBS +/-), which have a selective defect in homocysteine transsulfuration, and wild-type (CBS +/+) littermates were fed either a control diet or a diet that is relatively deficient in folic acid for 6 wk. Plasma total homocysteine was 5.3 +/- 0.7 microM in CBS +/+ mice and 6.4 +/- 0.6 microM in CBS +/- mice (P = 0.3) given the control diet. Plasma total homocysteine was 11.6 +/- 4.5 microM in CBS +/+ mice and 25.1 +/- 3.2 microM in CBS +/- mice (P = 0.004) given a low-folate diet. In mice fed the control diet, relaxation of aortic rings in response to the endothelium-dependent vasodilator acetylcholine did not differ significantly between CBS +/+ mice and CBS +/- mice. In contrast, in mice fed a low-folate diet, maximal relaxation to acetylcholine was markedly impaired in CBS +/- mice (58 +/- 9%) compared with CBS +/+ mice (84 +/- 4%) (P = 0.01). No differences in relaxation to the endothelium-independent vasodilator sodium nitroprusside were observed among the four groups of mice. These data indicate that CBS-deficient mice are predisposed to hyperhomocysteinemia during dietary folate deficiency, and moderate hyperhomocysteinemia is associated with marked impairment of endothelial function in mice.
Animals↗
Masked polycythaemia vera in a patient with extrahepatic portal venous obstruction.
Myeloproliferative disorder (MPD) is an important cause of thrombosis of the hepatic and portal venous system. The diagnosis in many of these patients is missed as they have an atypical clinical presentation and may have a normal haematological profile at presentation. We report a 30-year-old patient with features of portal hypertension due to extrahepatic portal venous obstruction. She had a normal haemoglobin level and haematocrit at presentation, but the red cell mass was found to be elevated even in the presence of low serum iron levels. A diagnosis of polycythaemia vera as the underlying disease was made.
Adult↗
Multilineage hemopoietic stem cell defects in Budd Chiari syndrome.
BACKGROUND/AIMS: Erythropoietin-independent endogenous growth of erythroid colony from bone marrow cells has been shown in many patients with Budd Chiari syndrome in earlier studies. In another report, increased megakaryocyte colony growth has also been documented in this disease. However, defects in granulocyte-macrophage cell lines in Budd Chiari syndrome have yet to be reported in the literature. METHODS: Both in vitro erythroid and granulocyte-macrophage colony cultures from peripheral blood mononuclear cells with and without erythropoietin or granulocyte-macrophage colony stimulating factor, respectively, were studied in 32 patients with Budd Chiari syndrome, along with 20 normal healthy controls and ten patient controls with portal hypertension (five patients each with noncirrhotic portal fibrosis and liver cirrhosis). In 18 patients the occlusion was only in the inferior vena cava, in five patients only in hepatic veins, and in nine patients both inferior vena cava and hepatic veins were blocked. RESULT: Endogenous erythroid or granulocyte-macrophage colony growth was not observed in any of the normal healthy controls or in patient controls with portal hypertension. However, 22 of the 32 (68.8%) patients showed endogenous erythroid colony growth. Moreover, four of them also showed endogenous growth of granulocyte-macrophage colony, not previously reported in Budd Chiari syndrome. CONCLUSION: It may be inferred that stem cell defects affecting all three hemopoietic cell lines (erythroid, megakaryocyte and granulocyte-macrophage) occur in Budd Chiari syndrome, which may be the primary defect responsible for the pro-thrombotic state causing venous thrombosis in them.
Budd-Chiari Syndrome↗
Overt polycythemia vera after splenopneumopexy in a patient with Budd-Chiari syndrome.
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Adult↗
Budd-Chiari syndrome: aetiology and geography.
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Budd-Chiari Syndrome↗
Polycythemia vera: overt to latent form in a patient with Budd-Chiari syndrome.
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Adult↗
Increased ratio of thromboxane B2 and 6-keto PGF1 alpha in patients of hepatic venous outflow obstruction.
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6-Ketoprostaglandin F1 alpha↗
Resistance to activated protein C (APC) in Indian patients of thrombophilia.
In a pilot study, 28 consecutive patients with thrombosis and 23 age and sex matched healthy normal controls were investigated with normalised APC sensitivity ratio (n-APC-SR) to know the defect exists and if so its prevalence in India. Six of the 28 (21.4%) thrombotic patients had n-APC-SR of < 0.76 (range 0.55 to 0.74) as compared to the normal control value (0.97 +/- 0.105). Our study shows APC resistance defect in a significant proportion (21.4%) of Indian patients with thrombotic disorders.
Adolescent↗
Platelet ultra-structure study in Budd-Chiari syndrome.
Morphologic characteristics of circulating platelets were studied in 20 patients with primary Budd-Chiari syndrome (BCS) without any known etiology, using transmission electron microscopy (TEM). Significant platelet ultrastructural changes were observed in all the patients (in 10-->90% platelets) as compared to 20 normal healthy controls (in up to 4% of their platelets). The prominent changes in the platelets were paucity or absence of alpha granules, hypertrophy of the open canalicular systems (OCS) and clumping and fusion of the granules and other organelles in the centre of platelets. Some other changes observed in platelets were dilated channels of OCS, pseudopodial protrusion of cytoplasm and presence of prominent masses of glycogen particles. Platelets from 20 normal controls processed along with the patients' platelets showed only a few such abnormalities. Most of these changes observed in patients' platelets were akin to the changes observed in platelets undergoing activation. Assay of plasma beta-thromboglobulin showed significantly higher levels in all the patients (p < 0.001) further confirming on-going in vivo platelet activation with morphologic changes most likely reflecting the thrombotic process present in BCS patients.
Adolescent↗
Kinetics and disposition of picumeterol in animals.
1. The pharmacokinetics and disposition of picumeterol, a novel beta 2 receptor agonist agent, have been studied in the rat and dog following administration by inhalation, intravenous and oral routes at various dose levels. 2. Picumeterol was found to be transferred across the lung of the rat and dog following inhalation dosage. After i.v. dosage picumeterol was eliminated from plasma with a half-life of about 1 h in the rat and about 2 h in the dog. Plasma clearance in the rat was about twice liver blood flow and the plasma levels of picumeterol were low after oral administration. 3. Following instillation of 14C-picumeterol to the trachea of isolated respiring rat lung preparations radioactivity was transferred from the airways to perfusion media as unchanged drug within 2 min. After 2 h perfusion, no metabolites were detected in the recirculation perfusate or lung. 4. Picumeterol was extensively metabolized in vivo in the rat (about 95%) and dog (about 90%) and in vitro in microsomal preparations of rat, dog and human liver. O-dealkylation and beta-oxidation are important as routes of metabolism. 5. Radioactivity was largely excreted in the urine of the rat and dog (> 50% of dose), as metabolites, following i.v. administration. There was some excretion of radioactivity in dog bile. Extensive first-pass metabolism was found after oral administration in the rat.
Administration, Inhalation↗