The Drosophila Nesprin-1 homolog MSP300 is required for muscle autophagy and proteostasis.

Nesprin proteins, which are components of the linker of nucleoskeleton and cytoskeleton (LINC) complex, are located within the nuclear envelope and play prominent roles in nuclear architecture. For example, LINC complex proteins interact with both chromatin and the cytoskeleton. Here, we report that the Drosophila Nesprin MSP300 has an additional function in autophagy within larval body wall muscles. RNAi-mediated MSP300 knockdown in larval body wall muscles resulted in defects in the contractile apparatus, muscle degeneration and defective autophagy. In particular, MSP300 knockdown caused accumulation of cytoplasmic aggregates that contained poly-ubiquitylated cargo, as well as the autophagy receptor ref(2)P (the fly homolog of p62 or SQSTM) and Atg8a. Furthermore, MSP300 knockdown larvae expressing an mCherry-GFP-tagged Atg8a transgene exhibited aberrant persistence of the GFP signal within these aggregates, indicating failure of autophagosome maturation. These autophagy deficits were similar to those exhibited by loss of the endoplasmic reticulum (ER) fusion protein Atlastin (Atl), raising the possibility that Atl and MSP300 might function in the same pathway. In support of this possibility, we found that a GFP-tagged MSP300 protein trap exhibited extensive localization to the ER. Alteration of ER-directed MSP300 might abrogate important cytoskeletal contacts necessary for autophagosome completion.

Electric-Field-Tunable Edge Transport in Bernal-Stacked Trilayer Graphene.

This Letter presents a nonlocal study on the electric-field-tunable edge transport in h-BN-encapsulated dual-gated Bernal-stacked (ABA) trilayer graphene across various displacement fields (D) and temperatures (T). Our measurements revealed that the nonlocal resistance (R_{NL}) surpassed the expected classical Ohmic contribution by a factor of at least 2 orders of magnitude. Through scaling analysis, we found that the nonlocal resistance scales linearly with the local resistance (R_{L}) only when the D exceeds a critical value of ∼0.2 V/nm. Additionally, we observed that the scaling exponent remains constant at unity for temperatures below the bulk-band gap energy threshold (T<25 K). Further, the value of R_{NL} decreases in a linear fashion as the channel length (L) increases. These experimental findings provide evidence for edge-mediated charge transport in ABA trilayer graphene under the influence of a finite displacement field. Furthermore, our theoretical calculations support these results by demonstrating the emergence of dispersive edge modes within the bulk-band gap energy range when a sufficient displacement field is applied.

Electric-Field-Tunable Valley Zeeman Effect in Bilayer Graphene Heterostructures: Realization of the Spin-Orbit Valve Effect.

We report the discovery of electric-field-induced transition from a topologically trivial to a topologically nontrivial band structure in an atomically sharp heterostructure of bilayer graphene (BLG) and single-layer WSe_{2} per the theoretical predictions of Gmitra and Fabian [Phys. Rev. Lett. 119, 146401 (2017)PRLTAO0031-900710.1103/PhysRevLett.119.146401]. Through detailed studies of the quantum correction to the conductance in the BLG, we establish that the band-structure evolution arises from an interplay between proximity-induced strong spin-orbit interaction (SOI) and the layer polarizability in BLG. The low-energy carriers in the BLG experience an effective valley Zeeman SOI that is completely gate tunable to the extent that it can be switched on or off by applying a transverse displacement field or can be controllably transferred between the valence and the conduction band. We demonstrate that this results in the evolution from weak localization to weak antilocalization at a constant electronic density as the net displacement field is tuned from a positive to a negative value with a concomitant SOI-induced splitting of the low-energy bands of the BLG near the K(K^{'}) valley, which is a unique signature of the theoretically predicted spin-orbit valve effect. Our analysis shows that quantum correction to the Drude conductance in Dirac materials with strong induced SOI can only be explained satisfactorily by a theory that accounts for the SOI-induced spin splitting of the BLG low-energy bands. Our results demonstrate the potential for achieving highly tunable devices based on the valley Zeeman effect in dual-gated two-dimensional materials.

Vanishing Thermal Equilibration for Hole-Conjugate Fractional Quantum Hall States in Graphene.

Transport through edge channels is responsible for conduction in quantum Hall (QH) phases. Robust quantized values of charge and thermal conductances dictated by bulk topology appear when equilibration processes become dominant. We report on measurements of electrical and thermal conductances of integer and fractional QH phases, realized in hexagonal boron nitride encapsulated graphite-gated bilayer graphene devices for both electron and hole doped sides with different valley and orbital symmetries. Remarkably, for complex edges at filling factors ν=5/3 and 8/3, closely related to the paradigmatic hole-conjugate ν=2/3 phase, we find quantized thermal conductance whose values (3κ_{0}T and 4κ_{0}T, respectively where κ_{0}T is the thermal conductance quantum) are markedly inconsistent with the values dictated by topology (1κ_{0}T and 2κ_{0}T, respectively). The measured thermal conductance values remain insensitive to different symmetries, suggesting its universal nature. Our findings are supported by a theoretical analysis, which indicates that, whereas electrical equilibration at the edge is established over a finite length scale, the thermal equilibration length diverges for strong electrostatic interaction. Our results elucidate the subtle nature of crossover from coherent, mesoscopic to topology-dominated transport.

CdSe- Reduced graphene oxide nanocomposite toxicity alleviation via V2O5 shell formation over CdSe core: in vivo and in vitro studies.

The present article demonstrates the synthesis of the nanocomposite of reduced graphene oxide (rGO) with CdSe and CdSe/V2O5 core/shell quantum dots by a two-step facile synthesis approach and subsequently studies their relative biocompatibility in different cells. Various characterization techniques have been applied including transmission electron microscopy (TEM), an x-ray diffractometer (XRD) and Raman spectroscopy to confirm the successful formation of CdSe-rGO and CdSe/V2O5-rGO nanocomposites. The average sizes of CdSe and CdSe/V2O5 QDs have found to be ∼3 and 5.5 nm, respectively with a good dispersion over the surface of rGO nanosheets. A crystal phase change has occurred during the formation of the V2O5 shell over the surface of CdSe QDs and confirmed through XRD. Raman spectroscopy has shown some useful insight of the surface state of CdSe and consequent changes in the surface with V2O5 shell growth. Further, MTT and cell growth assays have been performed to analyze their biocompatibility in A549 and Hela cells with various concentrations of as-synthesized materials. Our results demonstrate the toxicity of CdSe-rGO nanocomposite to be substantially reduced by the growth of the V2O5 shell. The in vivo studies in Drosophila show a remarkable decrease in the reactive oxygen species (ROS) and apoptosis levels for a CdSe/V2O5-rGO composite as compared to a CdSe-rGO nanocomposite, which paves a promising pathway for the CdSe/V2O5-rGO nanocomposite to be used as an efficient biocompatible material.

Folic acid supplementation rescues anomalies associated with knockdown of parkin in dopaminergic and serotonergic neurons in Drosophila model of Parkinson's disease.

parkin loss associated early-onset of Parkinson's disease, involves mitochondrial dysfunction and oxidative stress as the plausible decisive molecular mechanisms in disease pathogenesis. Mitochondrial dysfunction involves several up/down regulation of gene products, one of which being p53 is found to be elevated. Elevated p53 is involved in mitochondrial mediated apoptosis of neuronal cells in Parkinson's patients who are folate deficient as well. The present study therefore attempts to examine the effect of Folic acid (FA) supplementation in alleviation of anomalies associated with parkin knockdown using RNAi approach, specific to Dopaminergic (DA) neurons in Drosophila model system. Here we show that FA supplementation provide protection against parkin RNAi associated discrepancies, thereby improves locomotor ability, reduces mortality and oxidative stress, and partially improves Zn levels. Further, metabolic active cell status and ATP levels were also found to be improved thereby indicating improved mitochondrial function. To corroborate FA supplementation in mitochondrial functioning further, status of p53 and spargel was checked by qRT-PCR. Here we show that folic acid supplementation enrich mitochondrial functioning as depicted from improved spargel level and lowered p53 level, which was originally vice versa in parkin knockdown flies cultured in standard media. Our data thus support the potential of folic acid in alleviating the behavioural defects, oxidative stress, augmentation of zinc and ATP levels in parkin knock down flies. Further, folic acid role in repressing mitochondrial dysfunction is encouraging to further explore its possible mechanistic role to be utilized as potential therapeutics for Parkinson's disease.

Folic Acid Supplementation Ameliorates Oxidative Stress, Metabolic Functions and Developmental Anomalies in a Novel Fly Model of Parkinson's Disease.

Mutations in parkin cause early-onset Parkinson's disease. Studies involving Drosophila model have emphasised mitochondrial dysfunction as a critical event in disease pathogenesis. In this context, we employed a novel recessive allele of parkin, park (c00062) , for the current study. The piggyBac insertion at 3rd intron of parkin in park (c00062) was confirmed by PCR. Homozygous park (c00062) has diminished levels of truncated parkin transcript with no detectable protein as confirmed by qRT-PCR and western blot analysis, respectively. The homozygous park (c00062) displayed severe developmental anomalies involving reduced body size, ~45 % pupal lethality, high mortality with locomotory defect, elevated oxidative stress, low metabolic active cell status with low mitochondrial respiration as reflected from reduced ATP levels. Further, folic acid therapeutic potential was analysed in park (c00062) . Here we show that dietary folic acid provided protection against disparities involving pupal lethality, high mortality, locomotory defect, elevated oxidative stress and low metabolic active cell status associated with park (c00062) . Further mitochondrial respiration was enhanced as reflected from improved ATP levels in folate supplemented park (c00062) . To corroborate mitochondrial functioning further our analysis regarding transcript status of p53 and spargel by qRT-PCR, revealed down regulation of p53 and up regulation of spargel in folate supplemented park (c00062) , which was originally vice a versa. Our data thus support the potential of FA in alleviating the disparities associated with parkin loss of function in fly model. Further, FA role in alleviating mitochondrial dysfunction is encouraging to further explore FA mechanistic role to be utilized as potential therapeutics for parkin mediated neurodegenerative diseases.

Neonatal Intestinal Obstruction: Etiology, Management, and Outcomes in a Tertiary Care Center.

BACKGROUND:  Intestinal obstruction in neonates remains a critical medical emergency in the field of pediatric surgery. Clinical conditions often experience a sudden deterioration in their appearance. Multiple factors contribute to unfavorable clinical outcomes in underdeveloped nations. The study was conducted to identify the etiology, management, and outcomes of neonatal intestinal obstruction at a specialized medical facility. METHODS:  This retrospective study included 168 newborns who had to be operated on in the neonatal intensive care unit between 2021 and 2023 due to intestinal obstruction. The clinical and demographic characteristics of the infants, final diagnosis, surgical complications, and mortality rate were documented. In addition, the relationship between risk factors such as birth weight, gestational age, length of surgery, and postoperative problems was evaluated. RESULTS:  The majority of neonatal intestinal obstruction occurred within seven days of birth, with 8-15 days being the second most common. Most babies were born at full term (53.57%) and weighed 2 kg or more (75%). In newborns in our region, duodenal, ileal, jejunal, and colonic atresias were found to be the most common causes of neonatal intestinal obstruction that requires surgery. The study detected 45 postoperative problems, 26.79% of the total. Out of 168 patients, twelve (7.14%) had septicemia, seven (4.17%) had anastomotic leak, seven (4.17%) had aspiration pneumonitis, and two (1.19%) needed re-exploration. Overall mortality was 10.12%, with 17 patients dying. Moreover, 119 patients (70.83%) survived without issues, while 32 (19.05%) survived with complications. CONCLUSION:  Our findings emphasize the significance of promptly diagnosing, intervening, and implementing suitable management approaches to enhance outcomes for newborns with intestinal obstruction. Furthermore, it highlights valuable perspectives for healthcare professionals in enhancing care for this specific group of patients.

Motor neuron activity enhances the proteomic stress caused by autophagy defects in the target muscle.

Several lines of evidence demonstrate that increased neuronal excitability can enhance proteomic stress. For example, epilepsy can enhance the proteomic stress caused by the expression of certain aggregation-prone proteins implicated in neurodegeneration. However, unanswered questions remain concerning the mechanisms by which increased neuronal excitability accomplishes this enhancement. Here we test whether increasing neuronal excitability at a particular identified glutamatergic synapse, the Drosophila larval neuromuscular junction, can enhance the proteomic stress caused by mutations in the ER fusion/GTPase gene atlastin (atl). It was previously shown that larval muscle from the atl2 null mutant is defective in autophagy and accumulates protein aggregates containing ubiquitin (poly-UB aggregates). To determine if increased neuronal excitability might enhance the increased proteomic stress caused by atl2, we activated the TrpA1-encoded excitability channel within neurons. We found that TrpA1 activation had no effect on poly-UB aggregate accumulation in wildtype muscle, but significantly increased poly-UB aggregate number in atl2 muscle. Previous work has shown that atl loss from either neuron or muscle increases muscle poly-UB aggregate number. We found that neuronal TrpA1 activation enhanced poly-UB aggregate number when atl was removed from muscle, but not from neuron. Neuronal TrpA1 activation enhanced other phenotypes conferred by muscle atl loss, such as decreased pupal size and decreased viability. Taken together, these results indicate that the proteomic stress caused by muscle atl loss is enhanced by increasing neuronal excitability.

Atl (atlastin) regulates mTor signaling and autophagy in Drosophila muscle through alteration of the lysosomal network.

ABBREVIATIONS: atl atlastin; ALR autophagic lysosome reformation; ER endoplasmic reticulum; GFP green fluorescent protein; HSP hereditary spastic paraplegia; Lamp1 lysosomal associated membrane protein 1 PolyUB polyubiquitin; RFP red fluorescent protein; spin spinster; mTor mechanistic Target of rapamycin; VCP valosin containing protein.

Electrical noise spectroscopy of magnons in a quantum Hall ferromagnet.

Collective spin-wave excitations, magnons, are promising quasi-particles for next-generation spintronics devices, including platforms for information transfer. In a quantum Hall ferromagnets, detection of these charge-neutral excitations relies on the conversion of magnons into electrical signals in the form of excess electrons and holes, but if the excess electron and holes are equal, detecting an electrical signal is challenging. In this work, we overcome this shortcoming by measuring the electrical noise generated by magnons. We use the symmetry-broken quantum Hall ferromagnet of the zeroth Landau level in graphene to launch magnons. Absorption of these magnons creates excess noise above the Zeeman energy and remains finite even when the average electrical signal is zero. Moreover, we formulate a theoretical model in which the noise is produced by equilibration between edge channels and propagating magnons. Our model also allows us to pinpoint the regime of ballistic magnon transport in our device.

Mortality in patients with Coronavirus disease 2019 (COVID- 19) and its clinicoradiological and laboratory correlates: A retrospective study.

Aim: To delineate and analyze the mortality from COVID -19 in our institute during the devastating second wave of pandemic. Settings and Design: A retrospective cohort analysis. Methods and Materials: A comprehensive mortality analysis of 142 laboratory-confirmed severe acute respiratory syndrome coronavirus 2-infected deceased patients from our hospital's medical records was done. These patients presented with severe disease at the time of admission and were managed in intensive care units. Statistical Analysis Used: Statistical Package for Social Sciences software, IBM manufacturer, Chicago, USA, version 21.0 was used. Results: The number of deceased males (82, 62.6%) was higher than females (53, 37.3%). Median age of deceased patient was 57 (44.25-69.75) years. Most frequent comorbidities were diabetes mellitus (42, 29.6%) and hypertension (41, 28.9%). Most common symptoms being shortness of breath (137, 96.5%), fever (94, 66.2%) and cough (73, 51.4%). Median peripheral capillary oxygen saturation (SpO2) at time of admission was 86% (77.25-90). Median time interval from symptom onset to admission in hospital was 3 (2.25-5) days. Neutrophil lymphocyte ratio was more than 5 in 117 (90.7%) patients. Complications seen were acute respiratory distress syndrome in 82.3%, acute liver injury in 58.4%, acute kidney injury in 26.7%, sepsis in 13.3% and acute cardiac injury in 12% patients. The median high-resolution computed tomography score was 20 (17-22). Conclusions: Male and elderly patients with underlying comorbidities had poorer outcome and involvement of multiple organ systems was common. A short time interval between symptom onset and admission/mortality, particularly encountered was worrisome.

The Drosophila melanogaster attP40 docking site and derivatives are insertion mutations of msp-300.

The ɸC31 integrase system is widely used in Drosophila melanogaster to allow transgene targeting to specific loci. Over the years, flies bearing any of more than 100 attP docking sites have been constructed. One popular docking site, termed attP40, is located close to the Nesprin-1 orthologue msp-300 and lies upstream of certain msp-300 isoforms and within the first intron of others. Here we show that attP40 causes larval muscle nuclear clustering, which is a phenotype also conferred by msp-300 mutations. We also show that flies bearing insertions within attP40 can exhibit decreased msp-300 transcript levels in third instar larvae. Finally, chromosomes carrying certain "transgenic RNAi project" (TRiP) insertions into attP40 can confer pupal or adult inviability or infertility, or dominant nuclear clustering effects in certain genetic backgrounds. These phenotypes do not require transcription from the insertions within attP40. These results demonstrate that attP40 and insertion derivatives act as msp-300 insertional mutations. These findings should be considered when interpreting data from attP40-bearing flies.

Determination of topological edge quantum numbers of fractional quantum Hall phases by thermal conductance measurements.

To determine the topological quantum numbers of fractional quantum Hall (FQH) states hosting counter-propagating (CP) downstream (Nd) and upstream (Nu) edge modes, it is pivotal to study quantized transport both in the presence and absence of edge mode equilibration. While reaching the non-equilibrated regime is challenging for charge transport, we target here the thermal Hall conductance GQ, which is purely governed by edge quantum numbers Nd and Nu. Our experimental setup is realized with a hexagonal boron nitride (hBN) encapsulated graphite gated single layer graphene device. For temperatures up to 35 mK, our measured GQ at ν = 2/3 and 3/5 (with CP modes) match the quantized values of non-equilibrated regime (Nd + Nu)κ0T, where κ0T is a quanta of GQ. With increasing temperature, GQ decreases and eventually takes the value of the equilibrated regime ∣Nd - Nu∣κ0T. By contrast, at ν = 1/3 and 2/5 (without CP modes), GQ remains robustly quantized at Ndκ0T independent of the temperature. Thus, measuring the quantized values of GQ in two regimes, we determine the edge quantum numbers, which opens a new route for finding the topological order of exotic non-Abelian FQH states.

Observation of ballistic upstream modes at fractional quantum Hall edges of graphene.

The presence of "upstream" modes, moving against the direction of charge current flow in the fractional quantum Hall (FQH) phases, is critical for the emergence of renormalized modes with exotic quantum statistics. Detection of excess noise at the edge is a smoking gun for the presence of upstream modes. Here, we report noise measurements at the edges of FQH states realized in dual graphite-gated bilayer graphene devices. A noiseless dc current is injected at one of the edge contacts, and the noise generated at contacts at length, L = 4 µm and 10 µm away along the upstream direction is studied. For integer and particle-like FQH states, no detectable noise is measured. By contrast, for "hole-conjugate" FQH states, we detect a strong noise proportional to the injected current, unambiguously proving the existence of upstream modes. The noise magnitude remains independent of length, which matches our theoretical analysis demonstrating the ballistic nature of upstream energy transport, quite distinct from the diffusive propagation reported earlier in GaAs-based systems.

Observation of Time-Reversal Invariant Helical Edge-Modes in Bilayer Graphene/WSe2 Heterostructure.

Topological insulators, along with Chern insulators and quantum Hall insulator phases, are considered as paradigms for symmetry protected topological phases of matter. This article reports the experimental realization of the time-reversal invariant helical edge-modes in bilayer graphene/monolayer WSe2-based heterostructures-a phase generally considered as a precursor to the field of generic topological insulators. Our observation of this elusive phase depended crucially on our ability to create mesoscopic devices comprising both a moiré superlattice potential and strong spin-orbit coupling; this resulted in materials whose electronic band structure could be tuned from trivial to topological by an external displacement field. We find that the topological phase is characterized by a bulk bandgap and by helical edge-modes with electrical conductance quantized exactly to 2e2/h in zero external magnetic field. We put the helical edge-modes on firm ground through supporting experiments, including the verification of predictions of the Landauer-Büttiker model for quantum transport in multiterminal mesoscopic devices. Our nonlocal transport properties measurements show that the helical edge-modes are dissipationless and equilibrate at the contact probes. We achieved the tunability of the different topological phases with electric and magnetic fields, which allowed us to achieve topological phase transitions between trivial and multiple, distinct topological phases. We also present results of a theoretical study of a realistic model which, in addition to replicating our experimental results, explains the origin of the topological insulating bulk and helical edge-modes. Our experimental and theoretical results establish a viable route to realizing the time-reversal invariant Z2 topological phase of matter.

A selective D2 dopamine receptor agonist alleviates depression through up-regulation of tyrosine hydroxylase and increased neurogenesis in hippocampus of the prenatally stressed rats.

Prenatal stress (PNS) has its negative impact on both the infant hippocampal neurogenesis and pregnancy outcomes in the neonates that serves as a risk factor for postnatal depression in adult offsprings. Therefore, main objectives of the present study were to evaluate the effect of maternal chronic unpredictable mild stress (CUMS) on behavioural changes, levels of oxidative stress, changes in selective developmental signaling genes and neurogenesis in the adult brain of Wistar rats and its reversal through a selective non-ergoline D2 type dopamine receptor (D2R) agonist Ropinirole (ROPI). Effects of ROPI treatment on CUMS induced adult rats offspring were measured by assessment of behavioural tests (sucrose preference test and forced swim test), biomarkers of oxidative stress, protein expression of tyrosine hydroxylase (TH), mRNA expression of SHH, GSK-3ß, ß-catenin, Notch, brain-derived neurotrophic factor (BDNF), Dopamine receptor 2 (Drd2) and bromodeoxyuridine (BrdU) cell proliferation assay. The oxidative stress, protein and mRNA expression were determined in the hippocampus and prefrontal cortex while the BrdU cell proliferation was observed in the hippocampus of rat brain. PNS induced changes resulted in depression validated by the depression-like behaviours, increased oxidative stress, decreased TH expression, altered expression of selective developmental genes, along with the reduced hippocampal neurogenesis and BDNF expression in the brain of adult offsprings. Chronic ROPI treatment reversed those effects and was equally effective like Imipramine (IMI) treatment. So, the present study suggested that ROPI can be used as an antidepressant drug for the treatment of depressive disorders.

Piperine-Coated Gold Nanoparticles Alleviate Paraquat-Induced Neurotoxicity in Drosophila melanogaster.

Parkinson's disease (PD) is the most common progressive neurodegenerative disease known to impart bradykinesia leading to diverse metabolic complications. Currently, scarcity of effective drug candidates against this long-term devastating disorder poses a big therapeutic challenge. Here, we have synthesized biocompatible, polycrystalline, and uniform piperine-coated gold nanoparticles (AuNPspiperine) to specifically target paraquat-induced metabolic complications both in Drosophila melanogaster and SH-SY5Y cells. Our experimental evidence clearly revealed that AuNPspiperine can effectively reverse paraquat-induced lethal effects in both in vitro and in vivo model systems of PD. AuNPspiperine were found to suppress oxidative stress and mitochondrial dysfunction, leading to inhibition of apoptotic cell death in paraquat-treated flies. AuNPspiperine were also found to protect SH-SY5Y cells against paraquat-induced toxicity at the cellular level preferably by maintaining mitochondrial membrane potential. Both experimental and computational data point to the possible influence of AuNPspiperine in regulating the homeostasis of parkin and p53 which may turn out to be the key factors in reducing PD symptoms. The findings of this work may facilitate the development of piperine-based nanoformulations against PD.

Effects of chronic unpredictable mild stress induced prenatal stress on neurodevelopment of neonates: Role of GSK-3ß.

Prenatal stress (PNS) has gained attention with regard to its impact on hippocampal neurogenesis in neonates which serves as a risk factor for postnatal neurodevelopmental deficits. Evidences from animal models have suggested that depression responsive hypothalamic-pituitary-adrenal (HPA) axis and its hormonal response via cortisol, is responsible for critical neurodevelopmental deficits in the offspring which is transduced due to gestational stress. But knowledge in the area of assessing the effects of maternal chronic unpredictable mild stress (CUMS) on neurogenesis and expression of some key signaling molecules in the offsprings are limited. We have used Wistar rats to induce PNS in offsprings by maternal CUMS during pregnancy. Prefrontal cortex (PFC) and hippocampus were assessed for biomarkers of oxidative stress, neurogenesis, neurodevelopmental signaling molecules and DNA damage in the male Wister offsprings. Our investigations resulted in sufficient evidences which prove how maternal psychological stress has widespread effect on the fetal outcomes via major physiological alteration in the antioxidant levels, neurogenesis, signaling molecules and DNA damage. PNS leads to the upregulation of GSK-3ß which in turn inhibited mRNA and protein expressions of sonic hedgehog (SHH), ß-catenin, Notch and brain derived neurotrophic factor (BDNF). The study explored multifaceted signaling molecules especially, GSK-3ß responsible for crosstalks between different neurodevelopmental molecules like SHH, Notch, BDNF and ß-catenin affecting neurodevelopment of the offsprings due to PNS.

Universal quantized thermal conductance in graphene.

The universal quantization of thermal conductance provides information on a state's topological order. Recent measurements revealed that the observed value of thermal conductance of the 5 2 state is inconsistent with either Pfaffian or anti-Pfaffian model, motivating several theoretical articles. Analysis has been made complicated by the presence of counter-propagating edge channels arising from edge reconstruction, an inevitable consequence of separating the dopant layer from the GaAs quantum well and the resulting soft confining potential. Here, we measured thermal conductance in graphene with atomically sharp confining potential by using sensitive noise thermometry on hexagonal boron-nitride encapsulated graphene devices, gated by either SiO2/Si or graphite back gate. We find the quantization of thermal conductance within 5% accuracy for ν = 1 ; 4 3 ; 2 and 6 plateaus, emphasizing the universality of flow of information. These graphene quantum Hall thermal transport measurements will allow new insight into exotic systems like even-denominator quantum Hall fractions in graphene.