Vijay Kumar

Synthesis, electrochemical and optical properties of stable yellow fluorescent fluoranthenes.

A novel series of thermally stable yellow light emitting fluoranthenes with an amine donor and a nitrile acceptor was prepared from a ketene-S,S-acetal under mild conditions without using an organometal catalyst. The organic light emitting device of yellow fluoranthene 10b exhibited substantially low turn-on voltage (2.6 V) and maximum brightness of 470 Cd/m(2) with luminance efficiency of 2.0 Cd/A without using any dopant.

Non-aggregating solvatochromic bipolar benzo[f]quinolines and benzo[a]acridines for organic electronics

A novel series of light emitting and thermally stable non-aggregating benzannulated quinolines and acridines were designed and prepared from ketene-S,S-acetal under mild conditions through C–C bond formation. Photophysical and electrochemical analyses of these bipolar N-heterocyclic compounds revealed intense solvatochromism due to the intramolecular charge-transfer character, exemplary for 9b, which covered PL ranging from blue (480 nm) to green (501 nm) to yellow (562 nm) to orange (589 nm) using aprotic solvents of varying polarity. Organic light emitting devices with a device configuration of ITO/PEDOT:PSS (40 nm)/NPB (20 nm)/(N-heterocyclic compound) (50 nm)/BCP (7 nm)/LiF (0.7 nm)/Al (200 nm) were successfully prepared. The optoelectronic properties of these compounds were altered by controlled tuning of donor–acceptor and aromatic π-conjugation in benzo[f]quinolines and benzo[a]acridines, which exhibited a low turn-on voltage with electroluminescence ranging from blue (6c: λEL 455 nm) to green (8a: λEL 496 nm) to yellow (11: λEL 545 nm) to red (9b: λEL 630 nm).

Thermally Stable Nonaggregating Pyrenylarenes for Blue Organic Light-Emitting Devices†CDRI communication No. 8097.

A new series of thermally stable blue light-emitting nonplanar pyrenylarenes having an amine donor and a nitrile acceptor group was prepared from a ketene-S,S-acetal under conventional heating and/or microwave irradiation. The photophysical, electrochemical, and optical behavior of donor-acceptor pyrenylarenes are demonstrated. The performance of blue light-emitting pyrenylarenes was investigated by fabricating a multilayer device with the device configuration of ITO/PEDOT:PSS (40 nm)/NPB (30 nm)/pyrenylarene (55 nm)/BCP (8 nm)/LiF (0.6 nm)/Al (200 nm), which exhibited low turn-on voltage (5 V) with luminance efficiency of 0.8 Cd/A with nonaggregation behavior in both solution and solid state.

Transforming Growth Factor-Beta 1 (TGF-B1) Liberation from Its Latent Complex During Embryo Implantation and Its Regulation by Estradiol in Mouse

ABSTRACT Transforming growth factor-beta (TGF-B) plays an important role in embryo implantation; however, TGF-B requires liberation from its inactive latent forms (i.e., large latent TGF-B complex [LLC] and small latent TGF-B complex [SLC]) to its biologically active (i.e., monomer or dimer) forms in order to act on its receptors (TGF-BRs), which in turn activate SMAD2/3. Activation of TGF-B1 from its latent complexes in the uterus is not yet deciphered. We investigated uterine latent TGF-B1 complex and its biologically active form during implantation, decidualization, and delayed implantation. Our study, utilizing nonreducing SDS-PAGE followed by Western blotting and immunoblotting with TGF-B1, LTBP1, and latency-associated peptide, showed the presence of LLC and SLC in the uterine extracellular matrix and plasma membranous protein fraction during stages of the implantation period. A biologically active form of TGF-B1 (∼17-kDa monomer) was highly elevated in the uterine plasma membranous compartment at the peri-implantation stage (implantation and nonimplantation sites). Administration of hydroxychloroquine (an inhibitor of pro-TGF-B processing) at the preimplantation stage was able to block the liberation of biologically active TGF-B1 from its latent complex at the postimplantation stage; as a consequence, the number of implantation sites was reduced at Day 5 (1000 h), as was the number of fetuses at Day 13. The inhibition of TGF-B1 showed reduced levels of phosphorylated SMAD3. Further, the delayed-implantation mouse model showed progesterone and estradiol coordination to release the active TGF-B1 form from its latent complex in the receptive endometrium. This study demonstrates the importance of liberation of biologically active TGF-B1 during the implantation period and its regulation by estradiol.

Integrin Beta 8 (ITGB8) Regulates Embryo Implantation Potentially via Controlling the Activity of TGF-B1 in Mice

ABSTRACT Integrins (ITGs) are mediators of cell-cell and cell-matrix interactions, which are also associated with embryo implantation processes by controlling the interaction of blastocyst with endometrium. During early pregnancy, ITGbeta8 (ITGB8) has been shown to interact with latent transforming growth factor (TGF) beta 1 (TGFB1) at the fetomaternal interface. However, the precise role of ITGB8 in the uterus and its association with embryo implantation has not been elucidated. Therefore, we attempted to ascertain the role of ITGB8 during the window of embryo implantation process by inhibiting its function or protein expression. Uterine plasma membrane-anchored ITGB8 was augmented at peri-implantation and postimplantation stages. A similar pattern of mRNA expression was also found during the embryo implantation period. An immunolocalization study revealed the presence of ITGB8 on luminal epithelial cells along with mild expression on the stromal cells throughout the implantation period studied; however, an intense fluorescence was noted only during the peri- and postimplantation stages. Bioneutralization and mRNA silencing of the uterine Itgb8 at preimplantation stage reduced the rate/frequency of embryo implantation and subsequent pregnancy, suggesting its indispensable role during the embryo implantation period. ITGB8 can also regulate the liberation of active TGFB1 from its latent complex, which, in turn, acts on SMAD2/3 phosphorylation (activation) in the uterus during embryo implantation. This indicates involvement of ITGB8 in the embryo implantation process through regulation of activation of TGFB1.

Comparison of sea-level measurements between microwave radar and subsurface pressure gauge deployed at select locations along the coast of India

Abstract Sea-level data are obtained from several remote and coastal locations using absolute pressure gauges deployed at known level, known as chart datum. However, to yield correct sea-level measurements from absolute pressure measurements, it is necessary to take into account the atmospheric pressure and water density at the measurement locations. We used data collected from microwave radar and an absolute pressure gauge deployed at Verem, Goa (January 2009 to May 2010), Tuticorin, and Mandapam, Tamil Nadu (June 2010 to March 2011) to carry out comparative studies. The root-mean-square difference between the estimated sea level from radar and pressure gauge (incorporating atmospheric pressure correction) is ∼ 2.69 , 2.73, and 1.46 cm at Verem, Tuticorin, and Mandapam, respectively. Harmonic analysis of the two time-series of sea-level data at Verem produces similar residuals and tidal constituents. Our results indicate the importance of concurrent measurement of atmospheric pressure along with subsurface absolute pressure gauge measurements. Internet-based real-/near-real-time tracking and monitoring of sea level, sea state, and surface-meteorological conditions from a network of several island and coastal stations provides considerable information to disaster managers and local administrators during episodic events such as storms, storm surges, and tsunamis.

Integrin beta8 (ITGB8) activates VAV-RAC1 signaling via FAK in the acquisition of endometrial epithelial cell receptivity for blastocyst implantation

Integrin beta8 (ITGB8) is involved in the endometrial receptivity. The blastocyst first interacts with the luminal endometrial epithelial cells during its implantation; therefore, we have investigated the signaling of ITGB8 via FAK and VAV-RAC1 in the endometrial epithelial cells. Integrin beta8 was found elevated in epithelial cells at late-pre-receptive (day4, 1600 h) and receptive (day5, 0500 h) stages of endometrial receptivity period in the mouse. Integrins downstream molecule FAK has demonstrated an increased expression and phosphorylation (Y397) in the endometrium as well as in the isolated endometrial epithelial cells during receptive and post-receptive stages. Integrin beta8 can functionally interact with FAK, VAV and RAC1 as the levels of phosphorylated-FAK, and VAV along with the RAC-GTP form was reduced after ITGB8 knockdown in the endometrial epithelial cells and uterus. Further, VAV and RAC1 were seen poorly active in the absence of FAK activity, suggesting a crosstalk of ITGB8 and FAK for VAV and RAC1 activation in the endometrial epithelial cells. Silencing of ITGB8 expression and inhibition of FAK activity in the Ishikawa cells rendered poor attachment of JAr spheroids. In conclusion, ITGB8 activates VAV-RAC1 signaling axis via FAK to facilitate the endometrial epithelial cell receptivity for the attachment of blastocyst.

Endoglin (CD105) coordinates the process of endometrial receptivity for embryo implantation

Endoglin is a TGF-β receptor that is expressed in uterine endothelial and stromal cells in addition to trophoblast expression. However, the functional importance of endoglin in the embryo implantation process is not clear. We observed endoglin expression in the endometrium throughout the stages of its receptivity; however, its expression was enhanced during the receptive stage. Endoglin expression was predominant in epithelial cells of the lumen and glands, but showed a milder expression in stromal cells. Endoglin expression was initially observed in the primary decidual zone and later extended to the secondary decidua zone. Knockdown of endoglin via siRNA reduced the implantation sites along with the blastocyst numbers. Mouse blastocyst with endoglin-silenced endometrial epithelial cells (human and mouse origin) showed poor trophoblast outgrowth, which suggests an essential role for endoglin during endometrial receptivity. In conclusion, our findings reveal the association of endoglin with endometrial receptivity, which is important for embryo attachment.

Instrumentation for high-frequency meteorological observations from research vessel

Ship provides an attractive platform from which high-frequency meteorological observations (e.g., wind components, water vapor density, and air temperature) can be made accurately. However, accurate observations of meteorological variables depend on removal of shipmotion contaminations and appropriate placement of sensors onboard. Vertical and lateral wind components suffer more disturbances than longitudinal wind in consequence of ship motion. Wind stream approaching towards bow gets deflected due to the presence of ships superstructure that causes error in the wind measurements. It has been reported that underestimation in wind speed owing to the ships superstructure is ∼7% for bow-on wind and overestimation is ∼10% for relative wind direction of 900 [1]. Mean wind speed reduction of ∼8.5% were estimated due to the cylindrical mast when wind flows was parallel to the horizontal plane and excess of ∼9% for the wind flow normal to the plane. It has been observed that the effect of flow distortion on wind is less for relative wind direction of α450 relative to the major axis of the ship [2]. In this article, instrumentation used for measuring high-frequency components of meteorological parameters onboard Indian Research Vessel “Sindhu Sankalp” and correction of wind for ship motions is considered.

RHOG-DOCK1-RAC1 Signaling Axis Is Perturbed in DHEA-Induced Polycystic Ovary in Rat Model.

The function of RHOG, a RAC1 activator, was explored in the ovary during ovarian follicular development and pathological conditions. With the help of immunoblotting and immunolocalization, we determined the expression and localization of RHOG in normal (estrous cycle) and polycystic ovaries using Sprague Dawley (SD) rat model. Employing polymerase chain reaction and flow cytometry, we analyzed the transcript and expression levels of downstream molecules of RHOG, DOCK1, and RAC1 in the polycystic ovarian syndrome (PCOS) ovary along with normal antral follicular theca and granulosa cells after dehydroepiandrosterone (DHEA) supplementation. The effect of RHOG knockdown on DOCK1, VAV, and RAC1 expression was evaluated in the human ovarian cells (SKOV3), theca cells, and granulosa cells from SD rats with the help of flow cytometry. Oocyte at secondary follicles along with stromal cells showed optimal expression of RHOG. Immunoblotting of RHOG revealed its maximum expression at diestrus and proestrus, which was downregulated at estrus stage. Mild immunostaining of RHOG was also present in the theca and granulosa cells of the secondary and antral follicles. Polycystic ovary exhibited weak immunostaining for RHOG and that was corroborated by immunoblotting-based investigations. RHOG effectors DOCK1 and ELMO1 were found reduced in the ovary in PCOS condition/DHEA. RHOG silencing reduced the expression of DOCK1 and RAC1 in the theca and granulosa cells from SD rat antral follicles and that was mirrored in the human ovarian cells. Collectively, RHOG can mediate signaling through downstream effectors DOCK1 and RAC1 during ovarian follicular development (theca and granulosa cells and oocyte), but DHEA downregulated them in the PCOS ovary.The function of RHOG, a RAC1 activator, was explored in the ovary during ovarian follicular development and pathological conditions. With the help of immunoblotting and immunolocalization, we determined the expression and localization of RHOG in normal (estrous cycle) and polycystic ovaries using Sprague Dawley (SD) rat model. Employing polymerase chain reaction and flow cytometry, we analyzed the transcript and expression levels of downstream molecules of RHOG, DOCKI, and RACI in the polycystic ovarian syndrome (PCOS) ovary along with normal antral follicular theca and granulosa cells after dehydroepiandrosterone (DHEA) supplementation. The effect of RHOG knockdown on DOCKI, VAV, and RACI expression was evaluated in the human ovarian cells (SKOV3), theca cells, and granulosa cells from SD rats with the help of flow cytometry. Oocyte at secondary follicles along with stromal cells showed optimal expression of RHOG. Immunoblotting of RHOG revealed its maximum expression at diestrus and proestrus, which was downregulated at estrus stage. Mild immunostaining of RHOG was also present in the theca and granulosa cells of the secondary and antral follicles. Polycystic ovary exhibited weak immunostaining for RHOG and that was corroborated by immunoblotting-based investigations. RHOG effectors DOCK1 and ELMO1 were found reduced in the ovary in PCOS condition/DHEA. RHOG silencing reduced the expression of DOCK1 and RAC1 in the theca and granulosa cells from SD rat antral follicles and that was mirrored in the human ovarian cells. Collectively, RHOG can mediate signaling through downstream effectors DOCK1 and RAC1 during ovarian follicular development (theca and granulosa cells and oocyte), but DHEA downregulated them in the PCOS ovary.