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I Chakraborty

Publications and source records attributed to I Chakraborty.

16 recordsLinked to original sources
PubMed2005

Self-aggregation of alkyltrimethylammonium bromides (C10-, C12-, C14-, and C16TAB) and their binary mixtures in aqueous medium: a critical and comprehensive assessment of interfacial behavior and bulk properties with reference to two types of micelle formation.

The detailed interfacial adsorption and micellization behavior of pure and mixed alkyltrimethylammonium bromides (ATABs: C10-, C12-, C14-, and C16TAB) were studied using tensiometric, conductometric, fluorimetric, viscometric, and calorimetric methods. The critical micellar concentration (CMC), thermodynamics of adsorption and micellization, counterion binding, aggregation number, and micellar polarity were determined. It was observed that the studied 1:1 molar mixtures of C10-C12TAB, C10-C14TAB, and C10-C16TAB, and the mixtures C12-C14TAB and C12-C16TAB at different mole ratios produced two CMCs that were supported by the conductometric, calorimetric and viscometric methods. Compared to the first micelle, the second micelle condensed more counterions and produced a higher aggregation number, but their interior polarity states were the same. The surface excess, area minimum of the ATABs at the CMC and Gibbs free energy of adsorption were evaluated and compared. The ideality/nonideality states of the mixed micelles formed in solution were tested in the light of Clint and Rubingh's formalisms; the mixed systems were found to undergo moderate to weak synergistic interaction. The contributions of the terminal methyl group, the intermediate methylene groups, and the hydrophilic tetramethylammonium group toward the standard Gibbs free energy, enthalpy, and entropy of the micellization processes were deciphered and discussed.

Journal Article↗
PubMed2001

Oxygen atom transfer from nitrogenous ReVO reagents to diphosphines and subsequent transformations. Rhenium(III) products and reaction models.

The concerned diphosphines are Ph2P(CH2)nPPh2 (1), abbreviated PnP, and the ReVO reagents are ReOCl3L (2) and ReOCl3L' (3), where L and L' are the azopyridine and pyridine-imine ligands p-ClC6H4N=NC5H4N and p-MeC6H4N=CHC5H4N, respectively. One atom transfer from 2 to 1 has afforded Re(OPnP)Cl3L (4a, n = 1; 4b, n = 2; 4c, n = 3). Of these 4b and 4c are stable, but 4a undergoes spontaneous isomerization to Re(PlPO)Cl3L (5) in solution. Two-atom transfer studied with both 2 and 3 has afforded binuclear LCl3Re(OPnPO)ReCl3L (8a, n = 2; 8b, n = 3) and L'Cl3Re(OPnPO)ReCl3L' (9a, n = 2; 9b, n = 3) for n = 2, 3 and mononuclear Re(OP1PO)Cl3L (11) and Re(OP1PO)Cl3L' (12) for n = 1. The mixed system L'Cl3Re(OP2PO)ReCl3L (10) has been prepared from 3 and 4b. The complex Re(PPh3)Cl3L (7a) is furnished by the reaction of Re(OPPh3)Cl3L (6a) or 4b or 11 with PPh3. The species have been characterized with the help of spectral, electrochemical, and X-ray structural data. All the complexes have mer geometry except 5 and 7a, which have fac geometry. The latter is best suited for concurrent Re-N and Re-P back-bonding. Variable-temperature rate data of the reaction 4a-->5 are consistent with an intramolecular strongly associative transition state (delta S++, -22.6 eu) in which the dangling phosphine function lies close to the metal. Two-atom transfer to P1P is believed to proceed via a transient binuclear intermediate which undergoes cleavage at one end due to steric crowding, affording 11 and 12. Crystal data for the complexes are as follows: 5.1.5 C6H6, empirical formula C45H39Cl4N3OP2Re, crystal system triclinic, space group P1, a = 10.034(2) A, b = 10.737(2) A, c = 20.357(4) A, alpha = 89.38(3) degrees, beta = 87.79(3) degrees, gamma = 80.22(3) degrees, V = 2159.7(7) A3, Z = 2; 7a.CH2Cl2, empirical formula C30H25Cl6N3PRe, crystal system monoclinic, space group P2(1)/n, a = 11.695(6) A, b = 17.745(7) A, c = 15.459(9) A, beta = 100.94(5) degrees, V = 3150(3) A3, Z = 4; 9a, empirical formula C52H48Cl6N4O2P2Re2, crystal system monoclinic, space group C2/c, a = 19.769(12) A, b = 12.864(6) A, c = 22.20(2) A, beta = 101.76(6) degrees, V = 5530(6) A3, Z = 4; 11, empirical formula C36H30Cl4N3O2P2Re, crystal system monoclinic, space group I2/a, a = 16.866(6) A, b = 12.583(6) A, c = 34.78(2) A, beta = 99.22(4) degrees, V = 7285(7) A3, Z = 8.

Journal Article↗
PubMed2000

Evaluation of vitamin A status during pregnancy.

Adequate maternal vitamin A nutrition is essential for successful pregnancy outcome and estimation of serum retinol among pregnant women enables a precise and objective assessment of vitamin A status, during pregnancy, even in subclinical state. In order to evaluate vitamin A status during pregnancy, and its relationship with personal and pregnancy related variables of the mother, 300 antenatal clinic attenders were interviewed at RG Kar Medical College and Hospital, Calcutta and tested for serum retinol, using Carr-Price test. Serum retinol values less than 30 microg/dl and 20 microg/dl, in this study, were considered as poor and severe vitamin A deficiency respectively. According to this 14.7% and 4% pregnant women were found to be suffering from poor and severe vitamin A deficiency respectively. Clinical signs of vitamin A deficiency (eg, nightblindness) were reported only among 60% cases of the deficient population. The problems of vitamin A deficiency were associated with low literacy and poor nutritional status of the mother, advanced gestational age of current pregnancy,increased number of pregnancies, shorter interval between births and poor dietary intake of vitamin A rich foods during pregnancy. The study thus raises the question of supplementation of vitamin A, during pregnancy, in Indian context where habitual diets are either inadequate or deficient in vitamin A.

Adolescent↗
PubMed1997

Expression of vascular endothelial growth factor (VEGF) and VEGF-receptor messenger ribonucleic acids in the peri-implantation rabbit uterus.

The endometrial vasculature undergoes expansion during preimplantation stages and, even more prominently, after implantation. In addition to angiogenesis, vascular hyperpermeability accompanies the attachment and invasion of blastocysts into the uterine lining. Vascular endothelial growth factor (VEGF) is an angiogenic factor expressed in mammalian uteri that also has potent activity in inducing vascular permeability. Rabbit uteri were examined using Northern and in situ hybridization to assess the temporal and spatial expression of VEGF and its receptor (Flk-1, Flt-1) mRNAs during the pre- and peri-implantation periods (Days 0-8). Steady-state levels of VEGF mRNA were highest in endometrium at estrous and peri-implantation stages (Days 6-8). In situ hybridization revealed a shift from uniform expression of VEGF transcripts throughout the uterus at estrus and Day 4, to an endometrial epithelial localization just before and during implantation. At implantation sites, a pronounced signal was present in the trophoblastic knobs, the syncytial aggregates that attach to and invade the endometrium. VEGF protein was detected by immunoblot analysis in peri-implantation-stage uteri but was below the limit of detection in estrous endometrium. VEGF receptor mRNAs were expressed in the uterus at all stages examined, with high levels of Flk-1 and Flt-1 at estrus and again just before implantation, 6-3/4 days pregnant. The high level just before implantation correlates with in situ hybridization results showing a prominent, but transient, signal for Flk-1 mRNA in the endometrial epithelium. During implantation, Flk-1 mRNA was associated with blood vessels of the endometrial stroma. We conclude that VEGF is a candidate factor for the induction of vascular hyperpermeability at implantation in the rabbit and in the angiogenic process that follows.

Animals↗
PubMed1996

Developmental expression of the cyclo-oxygenase-1 and cyclo-oxygenase-2 genes in the peri-implantation mouse uterus and their differential regulation by the blastocyst and ovarian steroids.

Cyclo-oxygenase (COX) is a rate-limiting enzyme that converts arachidonic acid to prostaglandins (PGs) and exists in two isoforms, COX-1 and COX-2. In the rodent, increased uterine vascular permeability at sites of blastocyst apposition is one of the earliest prerequisite events in the implantation process. This event is preceded by generalized uterine edema and luminal closure, and coincides with the initial attachment reaction between the trophectoderm and luminal epithelium. Vasoactive PGs are implicated in these processes. Here we demonstrate that COX genes are differentially regulated in the peri-implantation mouse uterus. During the preimplantation period (days 1-4), the COX-1 gene was expressed in the uterine epithelium mainly on day 4 until the initiation of attachment reaction in the evening after which the expression was downregulated. This COX-1 expression coincides with the generalized uterine edema required for luminal closure. In contrast, the COX-2 gene was expressed in the luminal epithelium and subepithelial stromal cells at the anti-mesometrial pole exclusively surrounding the blastocyst at the time of attachment reaction on day 4 and persisted through the morning of day 5. This uterine gene was not expressed at the sites of blastocyst apposition during progesterone (P(4))-treated delayed implantation, but was readily induced in the uterus surrounding the activated blastocysts after termination of the delay by estradiol-17beta (E(2)). The results suggest that PG synthesis catalyzed by COX-2 is important for localized increased uterine vascular permeability and attachment reaction. The COX-1 gene that was downregulated from the time of attachment reaction on day 4 was again expressed in the mesometrial and anti-mesometrial secondary decidual beds on days 7 and 8. These results suggest that PGs generated by COX-1 are involved in decidualization and/or continued localized endometrial vascular permeability observed during this period. In contrast, the COX-2 gene, expressed at the anti-mesometrial pole on days 4 and 5, switched its expression to the mesometrial pole from day 6 onward. These results suggest that PGs produced at this site by COX-2 are involved in angiogenesis for the establishment of placenta. In the ovariectomized mice, the COX-1 gene was induced in the epithelium by a combined treatment with P(4) and E(2). However, P(4) and/or E(2) treatments failed to influence the uterine COX-2 gene. Overall, the results suggest that the uterine COX-1 gene is influenced by ovarian steroids, while the COX-2 gene is regulated by the implanting blastocyst during early pregnancy.

Amino Acid Sequence↗
PubMed1995

Cannabinoid ligand-receptor signaling in the mouse uterus.

Using RNA (Northern) blot hybridization and reverse transcription-PCR, we demonstrate that the brain-type cannabinoid receptor (CB1-R) mRNA, but not the spleen-type cannabinoid receptor (CB2-R) mRNA, is expressed in the mouse uterus and that this organ has the capacity to synthesize the putative endogenous cannabinoid ligand, anandamide (arachidonylethanolamide). The psychoactive cannabinoid component of marijuana--delta 9-tetrahydrocannabinol (THC)--or anandamide, but not the inactive and nonpsychoactive cannabidiol (CBD), inhibited forskolin-stimulated cyclic AMP formation in the mouse uterus, which was prevented by pertussis toxin pretreatment. These results suggest that uterine CB1-R is coupled to inhibitory guanine nucleotide-binding protein and is biologically active. Autoradiographic studies identified ligand binding sites ([3H]anandamide) in the uterine epithelium and stromal cells, suggesting that these cells are perhaps the targets for cannabinoid action. Scatchard analysis of the binding of [3H]WIN 55212-2, another cannabinoid receptor ligand, showed a single class of high-affinity binding sites in the endometrium with an apparent Kd of 2.4 nM and Bmax of 5.4 x 10(9) molecules per mg of protein. The gene encoding lactoferrin is an estrogen-responsive gene in the mouse uterus that was rapidly and transiently up-regulated by THC, but not by CBD, in ovariectomized mice in the absence of ovarian steroids. This effect, unlike that of 17 beta-estradiol (E2), was not influenced by a pure antiestrogen, ICI 182780, suggesting that the THC-induced uterine lactoferrin gene expression does not involve estrogen receptors. We propose that the uterus is a new target for cannabinoid ligand-receptor signaling.

Animals↗
PubMed1995

Expression and steroid hormonal control of Muc-1 in the mouse uterus.

Previous studies from our laboratory established that large M(r) mucin glycoproteins are major apically disposed components of mouse uterine epithelial cells in vitro. The present studies demonstrate that Muc-1 represents one of the apically disposed mucin glycoproteins of mouse uterine epithelia, and that Muc-1 protein and messenger RNA (mRNA) expression are regulated in the periimplantation mouse uterus by ovarian steroids. Muc-1 expression is exclusive to the epithelial cells of the uterus under all conditions examined. Muc-1 expression is high in the proestrous and estrous stages and decreases during diestrous. Both Muc-1 protein and mRNA decline to barely detectable levels by day 4 of pregnancy, i.e. before the time of blastocyst attachment. In contrast, Muc-1 expression in the cervix and vagina is maintained during this same period. Delayed implantation was established in pregnant mice by ovariectomy and maintained by the administration of exogenous progesterone (P). Initiation of implantation was triggered by coinjection of P-maintained mice with a nidatory dose of 17 beta-estradiol (E2). Muc-1 levels in the uterine epithelia of P-maintained mice declined to low levels similar to those observed on day 4 of normal pregnancy. Coinjection of E2 did not alter Muc-1 expression, suggesting that down-regulation of Muc-1 is a P-dominated event. This was confirmed in ovariectomized nonpregnant mice, which displayed stimulation of Muc-1 expression after 6 h of E2 injection. E2-Stimulated Muc-1 expression was inhibited by the pure antiestrogen, ICI 164,384. Although P alone had no effect on Muc-1 expression, it antagonized the action of E2. Injection of pregnant mice with the antiprogestin, RU486, a known implantation inhibitor, on day 3 of pregnancy restored high level expression of Muc-1 mRNA on day 4, indicating that down-regulation of Muc-1 is P receptor mediated. Collectively, these data indicate that Muc-1 expression in mouse uterine epithelium is strongly influenced by ovarian steroids. It is suggested that the loss of Muc-1 contributes to generation of a receptive uterine state.

Animals↗
PubMed1995

Amphiregulin is an implantation-specific and progesterone-regulated gene in the mouse uterus.

A synchrony between the activated state of the blastocyst and differentiation of the uterus to the receptive state is essential to the process of implantation. This process is directed by progesterone (P4) and estrogen. The mechanism by which P4 differentiates the uterus, enabling estrogen to initiate implantation, is unknown but likely to involve localized induction of growth and differentiation factors. We have cloned the murine amphiregulin (AR) gene, a newly discovered member of the epidermal growth factor family, and demonstrate that its expression is implantation-specific and P4-regulated in the mouse uterus. A transient surge in AR mRNA levels occurred throughout the uterine epithelium on day 4 of pregnancy. With the onset of blastocyst attachment late on day 4, AR mRNA accumulated in the luminal epithelium exclusively at the sites of blastocysts. Thus, AR expression correlated first with rising P4 levels and then with the attachment reaction. The rapid induction of AR mRNA in the ovariectomized uterus only by P4 and abrogation of this induction by RU-486 (a P4 receptor antagonist) suggest that this uterine gene is regulated by P4. AR appeared to exhibit preferential phosphorylation of epidermal growth factor receptor in the uterus over that in the blastocyst. This is a first report of a P4-regulated uterine epithelial cell growth factor that is associated with epithelial cell differentiation during implantation. The association of AR in implantation is further documented by its down-regulation in the day 4 pregnant uterus in which uterine receptivity and implantation were disrupted by estrogen or RU-486 treatment on day 3. These results further indicate that the expression of the AR gene could serve as a molecular marker for the receptive state of the uterus for implantation.

Amino Acid Sequence↗
PubMed1995

Differential expression of vascular endothelial growth factor and its receptor mRNAs in the mouse uterus around the time of implantation.

Vascular endothelial growth factor (VEGF) is a mitogen for endothelial cells and an inducer of angiogenesis. VEGF is also known as a vascular permeability factor because it can stimulate vascular permeability. In the rodent, increased uterine vascular permeability occurs at the sites of blastocysts with the onset of the attachment reaction. This is followed by stromal decidualization and angiogenesis. We examined the temporal and spatial expression of VEGF and its receptors, Flk-1 and Flt-1, in the mouse uterus during the peri-implantation period (days 1-8) using Northern and in situ hybridization to assess the involvement of VEGF in the process of implantation. Primarily, a major (approximately 4.2 kb) transcript for VEGF mRNA was detected in uterine poly(A)+ samples, except for the presence of two other minor (approximately 3.7 and 2.5 kb) transcripts in decidual samples. The steady-state levels of these transcripts did not vary much during the peri-implantation period, except for an increase in day-8 decidual samples. Results of in situ hybridization experiments demonstrated accumulation of VEGF mRNA in the luminal epithelium on days 1 and 2. In contrast, stromal cells exhibited a modest level of signals on day 3. On day 4, luminal epithelial cells and those in the subepithelial stromal bed accumulated VEGF mRNA. On days 5-7, a clear cell type-specific accumulation of this mRNA was noted. On day 5 after the initial attachment reaction, luminal epithelial and stromal cells immediately surrounding the blastocyst exhibited accumulation of VEGF mRNA. On days 6-8, the accumulation occurred in cells in the decidual bed at both the mesometrial and antimesometrial poles. The embryo, especially the trophoblast giant cells, also accumulated VEGF mRNA on day 8. The expression of the VEGF receptors, Flk-1 and Flt-1, was also examined. A single transcript (approximately 6.5-7.0 kb) for Flk-1 mRNA and two transcripts (approximately 6.5 and 7.5 kb) for that of Flt-1 were detected in poly(A)+ uterine RNA samples. In situ hybridization studies showed accumulation of Flk-1 mRNA in a subset of cells in the stromal bed on day 4, but not in any uterine cell types on day 1. On days 5-8, cells in both the mesometrial and antimesometrial decidual beds exhibited accumulation of Flk-1 and Flt-1 mRNAs. Lectin binding (Dolichos biflorus agglutinin) was used to identify newly sprouting endothelial cells (angiogenesis), while an antibody to the von Willebrand factor (vWF) was employed to identify endothelial cells in general.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Modulation of sialic acid-binding proteins of rat uterus in response to changing hormonal milieu.

A group of sialic acid binding (SAS) agglutinins has been isolated from the rat uteri at different stages [Proestrus (P), estrus (E) and diestrus (D)] of estrous cycle. Studies of biochemical properties indicate that SAS agglutinins are glycoprotein in nature having molecular weights between 28-31 Kd and microheterogenous pI. Function-based characterization revealed that inspite of the fact that all three proteins exhibit sialic acid binding property, the sialic acid binding affinities, calculated from Scatchard analysis, using 4-methylumbelliferyl sialic acid as a ligand, varied in stage specific manner (Ka:D-SAS-9.03 x 10(5) M-1, P-SAS-2.33 x 10(5) M-1, E-SAS-2.13 x 10(5) M-1). Circular dichroism spectra of these three agglutinins suggested that differences exist in the secondary structures of the proteins isolated from different stages. Removal of carbohydrate moiety by trifluoromethane sulfonic acid treatment and CNBr cleavage studies showed some homology between these proteins, however, the variation in the carbohydrate moiety was apparent from the sugar analysis data. Functionally and immunologically these proteins can be grouped as estrogenic and progestogenic SAS agglutinins.

Agglutinins↗
PubMed1993

Hormonal regulation of sialic acid-binding (SAS) protein synthesis of rat uterus.

Sialic acid binding proteins (SAS) of rat uteri have been found in all three stages of the estrous cycle. To study the control of synthesis of these proteins two different animal models were used I-immature female rats (25 d) where the hormones estradiol (E2) and progesterone (P4) were given separately and together, and II-adult female rats where hormone treatment commenced 14 days after ovariectomy. The data indicated that E2 initiated the synthesis of SAS proteins in the immature animals, while P4 could inhibit SAS synthesis, either given alone or together with E2. However, prior priming of the rat with E2 and subsequent administration of P4 stimulated SAS protein synthesis.

Agglutinins↗
PubMed1987

Antagonistic and synergistic effects of lead and selenium in Rattus norvegicus.

Female rats were administered intraperitoneal injections of solutions of lead acetate and sodium selenite. The salt solutions were given singly to 'control' animals and successively to the 'treated' animals in both chronic and acute treatments but with or without a time gap of 1 h in the latter treatment. In the chronic treatments the dosage of lead acetate was kept constant and that of sodium selenite varied while in the acute treatments the ratio of the two salts was kept constant. Degrees of protection afforded by sodium selenite against chromosomal damage caused by lead acetate were assessed.

Animals↗
PubMedDate not supplied

Iodine deficiency disorders among school children of Dakshin Dinajpur District, West Bengal.

Iodine deficiency disorders (IDD) are major public health problems in India, including West Bengal. Existing programme to control IDD needs to be continuously monitored through recommended methods and indicators. Thus we undertook the study to assess the prevalence of goiter, status of urinary iodine excretion (UIE) level and to estimate iodine content of salts at the household level in Dakshin Dinajpur district, West Bengal. We conducted a community-based, cross-sectional study in 2004; among 2250 school children, aged 8-10 years. The '30 cluster' sampling methodology and indicators for assessment of IDD, as recommended by the joint WHO/UNICEF/ICCIDD consultation, were used for the study. Goitre was assessed by standard palpation technique, UIE was analyzed by wet digestion method and salt samples were tested by spot iodine testing kit. Of the 2250 children, 419 (18.6%) had goitre (95% CI = 17.0 - 20.2%). Total goitre rate (TGR) was not significantly different in respect of gender, age and religion. Visible goitre rate was 2.5%. Median urinary iodine excretion level was 16 mcg/dL (normal: > or = 10 mcg/dl.) and 16.5% children had value less than 5 mcg/dL. Only 67.4% of the salt samples tested had adequate iodine content of > or = 15 ppm, with significant difference between Hindus and Muslims (chi2 = 12.68, d.f. = 1, p < 0.01). TGR of 18.6% indicate the district is still endemic for IDD, but median urinary iodine within normal range reflects no current iodine deficiency. The district is in the transition phase from iodine-deficient to iodine-sufficient. Measures are to be sustained for successful transition towards elimination.

Child↗