Improvement of atmospheric pollution in the capital cities of US during COVID-19.

The spread of COVID-19 during 2020 impacted the whole world and still affecting the lives of people living in some parts of the world. The spread of this epidemic started in the US in late March 2020 and became a major issue in April due to an outburst of COVID-19 cases. Most of the countries in the world imposed complete to partial lockdown, but in the US, few states imposed lockdowns. Even after the advisory of the various Government department, the mobility data suggest that there was an enhancement (10-15%) in mobility during March 2020. Later sudden drop in mobility was observed during April 2020. The fall in aerosols optical depth (AOD), particulate matter concentration, NO2, and Ozone are observed along with the positive shifts in the SO2. In some of the states, AOD shows pronounced decline during May and June (5-40.90%), in the month of  May more than 80% decline was observed compared to the month of June 2020. In the month of April 2020, up to 73.64% decline was observed in NO2, and 70-99% in the months of May and June 2020. We found a good relationship between the mobility data and improvement in the air quality of the US. The changes were not significant compared to other countries in the world due to scattered lockdown policy, but in the US a pronounced change is observed during April month compared to March and May.

The impact of fluence dependent 120 MeV Ag swift heavy ion irradiation on the changes in structural, electronic, and optical properties of AgInSe2 nano-crystalline thin films for optoelectronic applications.

Swift heavy ion (SHI) irradiation in thin films significantly modifies the structure and related properties in a controlled manner. In the present study, the 120 MeV Ag ion irradiation on AgInSe2 nanoparticle thin films prepared by the thermal evaporation method and the induced modifications in the structure and other properties are being discussed. The ion irradiation led to the suppression of GIXRD and Raman peaks with increasing ion fluence, which indicated amorphization of the AgInSe2 structure along the path of 120 MeV Ag ions. The Poisson's fitting of the ion fluence dependence of the normalized area under the GIXRD peak of AgInSe2 gave the radius of the ion track as 5.8 nm. Microstructural analysis using FESEM revealed a broad bi-modal distribution of particles with mean particle sizes of 67.5 nm and 159 nm in the pristine film. The ion irradiation led to the development of uniform particles on the film surface with a mean size of 36 nm at high ion fluences. The composition of the film was checked by the energy dispersive X-ray fluorescence (EDXRF) spectrometer. The UV-visible spectroscopy revealed the increase of the electronic bandgap of AgInSe2 films with an increase in ion fluence due to quantum confinement. The Hall measurement and EDXRF studies showed that the unirradiated and irradiated AgInSe2 films have n-type conductivity and vary with the ion fluence. The changes in the films were tuned with different ion fluence and are favorable for both optical and electronic applications.

Sensitivity of Anatase and Rutile Phases of TiO2 to ion irradiation: Examination of the applicability of Coulomb Explosion and Thermal Spike Models.

Sensitivity of the anatase and rutile phases of titanium dioxide to Swift Heavy Ion (SHI) irradiation was experimentally probed and compared with the predictions of the Coulomb explosion, analytical and inelastic thermal spike models of ion-matter interaction. Conforming to the predictions of all these models, our study indicated higher sensitivity of anatase to these ions than the rutile phase. A detailed examination however revealed that Coulomb explosion model cannot explain either the nature of variation of the interaction cross section of SHI with the energy deposited by these ions, Se to the target electrons, or the relative values of the threshold electronic energy loss, Seth of anatase and rutile. The analytical thermal spike (a-TS) model, using the available physicochemical data for this oxide, predicted that tracks cannot form either in anatase or in rutile by 297 MeV and 511 MeV Ni ions, while inelastic thermal spike (i-TS) model predicted formation of ion tracks by 297 MeV Ni ions and their absence with 511 MeV Ni ions in both anatase and rutile. Our observation agreed with the predictions of i-TS model albeit with a difference in the radius of the tracks. In addition, we observed halo of defect ridden crystalline region of much larger radius around the ion track. Interestingly, the radius of the halo scales with the velocity of the ions, which is opposite to the conventionally observed velocity effect.

Anomalous x-ray diffraction peak broadening and lattice strains in Zn(1-x)Co(x)O dilute magnetic semiconductors.

Nanocrystalline powders of Zn(1-x)Co(x)O synthesized by the coprecipitation technique show anomalous anisotropic broadening for x>0.05. This peak broadening is shown to be not only due to a reduction in the particle size but also due to a significant strain contribution, as confirmed by Williamson-Hall analysis. The presence of grouped Co(2+) ions, revealing the presence of clusters of high spin Co(2+) with antiferromagnetically coupled spins, as indicated by magnetization studies, seems to be responsible for the strain.

Targeting of protein kinase C delta to mitochondria in the oxidative stress response.

The cellular response to oxidative stress includes the release of mitochondrial cytochrome c and the induction of apoptosis. Here we show that treatment of diverse cells with hydrogen peroxide (H2O2) induces the targeting of protein kinase C delta (PKCdelta) to mitochondria. The results demonstrate that H2O2-induced activation of PKCdelta is necessary for translocation of PKCdelta from the cytoplasm to the mitochondria. The results also show that mitochondrial targeting of PKCdelta is associated with the loss of mitochondrial transmembrane potential and release of cytochrome c. The functional importance of this event is also supported by the demonstration that H2O2-induced apoptosis is blocked by the inhibition of PKCdelta activation and translocation to mitochondria. These findings indicate that mitochondrial targeting of PKCdelta is required, at least in part, for the apoptotic response of cells to oxidative stress.

Mitochondrial targeting of JNK/SAPK in the phorbol ester response of myeloid leukemia cells.

Treatment of human U-937 myeloid leukemia cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with activation of the stress-activated protein kinase (SAPK) and induction of terminal monocytic differentiation. The present studies demonstrate that TPA targets SAPK to mitochondria by a mechanism dependent on activation of protein kinase C (PKC) beta. Translocation of SAPK to mitochondria in response to TPA is associated with release of cytochrome c, caspase-3 activation and induction of apoptosis. The results show that TPA induces the association of SAPK with the mitochondrial anti-apoptotic Bcl-x(L) protein. Overexpression of Bcl-x(L) attenuated the apoptotic response to TPA treatment. Moreover, expression of Bcl-x(L) mutated at sites of SAPK phosphorylation (Thr-47, -115) was more effective than wild-type Bcl-x(L) in abrogating TPA-induced cytochrome c release and apoptosis. By contrast, expression of Bcl-x(L) had little effect on induction of the monocytic phenotype. These findings indicate that myeloid leukemia cells respond to TPA with targeting of SAPK to mitochondria and that this response contributes to terminal differentiation through the release of cytochrome c and induction of apoptosis.

Targeting of the c-Abl tyrosine kinase to mitochondria in the necrotic cell death response to oxidative stress.

The ubiquitously expressed c-Abl tyrosine kinase is activated in the response of cells to genotoxic and oxidative stress. The present study demonstrates that reactive oxygen species (ROS) induce targeting of c-Abl to mitochondria. We show that ROS-induced localization of c-Abl to mitochondria is dependent on activation of protein kinase C (PKC)delta and the c-Abl kinase function. Targeting of c-Abl to mitochondria is associated with ROS-induced loss of mitochondrial transmembrane potential. The results also demonstrate that c-Abl is necessary for ROS-induced depletion of ATP and the activation of a necrosis-like cell death. These findings indicate that the c-Abl kinase targets to mitochondria in response to oxidative stress and thereby mediates mitochondrial dysfunction and cell death.

Genetic analysis of the in vivo role of DNA polymerases in Saccharomyces cerevisiae.

In Saccharomyces cerevisiae, the suggested functions of DNA polymerases (DNApol) have been based primarily on the characterization of the wild-type and mutant enzymes via in vitro studies. Here we describe a novel replication system to decipher the role of different DNA polymerases in in vivo DNA replication. Using this system, [alpha-32P]dNTP is allowed to cross the membrane of permeabilized cells; then the nature of the radiolabeled products of DNA synthesis is analyzed by gel electrophoresis and densitometry. Results of such analyses show that these replication intermediates are synthesized in the range 50-1,300 bp, which are then rapidly elongated and then ligated into longer DNA chains, and that the in vivo synthesis of yeast DNA fragments is dependent essentially on DNApolalpha and DNApoldelta, but not necessarily on DNApolepsilon. Results presented here support the views that DNApolepsilon is dispensable for yeast DNA replication or that DNA polalpha and DNApoldelta are epistatic to DNApolepsilon in yeast.

Inhibitory effect of piceatannol, a protein tyrosine kinase inhibitor, on asexual maturation of Plasmodium falciparum.

This report describes the effect of piceatannol (3,4,3',5'-tetrahydroxy trans stilbene), a plant secondary natural product, on protein tyrosine kinase (PTK) activity in different stages of P. falciparum grown in vitro. Piceatannol inhibited PTK activity in trophozoites and schizonts suggesting that PTK may be important in the initial asexual maturation of the parasite. Inhibition of PTK activity by piceatannol may thus provide new insights into more specific tools for chemotherapeutic interventions for P. falciparum.

Inhibition of a protein tyrosine kinase activity in Plasmodium falciparum by chloroquine.

The aim of the present study was to establish the importance of phosphorylation events for parasite growth and maturation. Investigations into the cytosolic Plasmodium falciparum protein tyrosine kinase (PTK) activity revealed that there is a stage specific increase in the activity, in the order ring < trophozoite < schizont in both chloroquine sensitive (CQ-S) and chloroquine resistant (CQ-R) strains (p < 0.05). Our data also show that in vivo conversion of the schizont stage to ring stage via release of merozoites is associated with a decrease in PTK activity. Piceatannol, a specific inhibitor of PTK inhibited the activity in both the CQ-S and CQ-R strains of the parasites. The presence of low levels of chloroquine (CQ) inhibited the cytosolic PTK activity in a dose dependent manner (IC50 = 45 mumoles or 23 micrograms/ml) in CQ-S strains. The effect of varying concentration of CQ on the kinetics of peptide phosphorylation reveal that CQ was a competitive inhibitor of PTK with respect to peptide substrate and non-competitive with respect to ATP indicating that CQ inhibits PTK activity by binding with protein substrate binding site. These data thus suggests that maturation of malaria parasite may be due to this cellular PTK and its inhibition by CQ could provide a hypothesis to explain its antimalarial activity and efficacy.

An aphidicolin-resistant mutant of Chinese hamster ovary cell with altered DNA polymerase and 3' exonuclease activities.

A comparison was made of partially purified DNA polymerases alpha, delta, epsilon and from normal Chinese hamster ovary cells and mutant cells (JK3-1-2A) resistant to aphidicolin, araA, and araC. In vitro the pol alpha from the mutant cells (1) was resistant to aphidicolin and araCTP but was sensitive to araATP, (2) showed a 1.6 to 2.6-fold reduced specific activity, and (3) was more sensitive to carbonyldiphosphonate, DMSO and SJK 287-38 anti-pol alpha antibody inhibition, but was less sensitive to alkylphenyl nucleotide analogs BuPdGTP and BuAdATP. On the other hand, pol delta and pol epsilon of the mutant cells did not show increased aphidicolin-resistance but differed from the wild type enzymes with regard to their 3' exonuclease activity. The 3' exonuclease/DNA polymerase activity ratio was increased 6-fold for pol delta and 3.3-fold for pol epsilon for enzymes from the mutant cells in comparison to wild type values. It is suggested that these altered properties of the DNA polymerases of the alpha-family are responsible for in vivo aphidicolin resistance of the mutant cells. The higher 3' exonuclease activity may explain the observed antimutator phenotype of this cell line. In view of the proficient 3' exonuclease activities of the DNA pol delta and epsilon, the present aphr mutant is unique among all mammalian DNA polymerase mutants.

Genetic evidence that aphidicolin inhibits in vivo DNA synthesis in Chinese hamster ovary cells.

Using a genetic approach, Chinese hamster ovary (CHO) cells sensitive (aphS) and resistant (aphR) to aphidicolin were grown in the presence or absence of various DNA polymerase inhibitors, and the newly synthesized DNA isolated from [32P]dNMP-labelled, detergent-permeabilized cells, was characterized after fractionation by gel electrophoresis. The particular aphR mutant CHO cell line used was one selected for resistance to aphidicolin and found to possess an altered DNA polymerase of the alpha-family. The synthesis of a 24 kb replication intermediate was inhibited in wild-type CHO cells grown in the presence of aphidicolin, whereas the synthesis of this replication intermediate was not inhibited by this drug in the mutant CHO cells or in the aphidicolin-resistant somatic cell hybrid progeny constructed by fusion of wild-type and mutant cell lines. Arabinofuranosylcytosine (ara-C), like aphidicolin, inhibited the synthesis of this 24 kb DNA replication intermediate in the wild-type CHO cells but not in the aphR mutant cells. However, carbonyldiphosphonate (COMDP) inhibited the synthesis of the 24 kb replication intermediate in both wild-type and mutant cells. N2-(p-n-Butylphenyl)-2' deoxyguanisine-5'-triphosphate (BuPdGTP) was found to inhibit the formation of Okazaki fragments equally well in the wild-type and mutant cell lines and thus led to inhibition of synthesis of DNA intermediates in both cases. It appears that aphidicolin and ara-C both affect a common target on the DNA polymerase, which is different from that affected by COMDP in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

Receptor heterogeneity and invasion on erythrocytes by Plasmodium falciparum merozoites in Indian isolates.

Malarial parasites, P. falciparum with different capabilities of invasion on sialic acid deficient erythrocytes have been identified. All three parasite lines (FDL-RI; FSJ-B5; FJB-D2) required sialic acid for invasion. However, parasite FSJ-B5 cultured in neuraminidase treated erythrocytes invaded at 20% efficiency, whereas in the cells treated with neuraminidase and trypsin together, the parasites FDL-R1 and FJB-D2 invaded at less than 10% efficiency. It is therefore suggested that different parasites isolated from different geographical regions of India possess two receptors--one that binds at sialic acid dependent ligand and other that binds in sialic acid independent ligand as demonstrated by ELISA using monoclonals against glycophorin A and glycophorin B. The sialic acid independent ligand may be having different affinities of their receptors for the malarial parasites.

Oxidative stress and malaria-infected erythrocytes.

This paper presents several mechanisms/pathways by which oxidative stress could cause damage to the parasites. During developmental stages of plasmodia profound alterations of the structure and function of host erythrocytes take place, in order to support the development and/or survival of the parasite. In addition an oxidant stress is also induced by the parasite. There is also an increased production of reactive oxygen species (ROS) by the parasite. This may deplete the erythrocyte of its defense mechanisms namely, superoxide dismutase (SOD), catalase, glutathione peroxidase, NADPH, NADH, glutathione (GSH) and glutathione reductase etc. Thus oxidative stress may be exerted by the growing parasite in red blood cells which are highly sensitive to such a challenge. These enhanced alterations may result in a retarded development of the parasite. Thus, the coexistence of both parasite and erythrocyte is a matter of a delicate balance. However, one cannot rule out the role of external modulations (immune pressure) inhibiting the vitality of the parasites.

Aphidicolin-resistant Chinese hamster ovary cells possess altered DNA polymerases of the alpha-family.

DNA polymerases alpha, delta and epsilon were partially purified and characterized from a wild type Chinese hamster ovary (CHO) cell line and from two aphidicolin-resistant mutant CHO cell lines (BR5 and BR5-20a). The main characteristics of the wild type and mutant DNA polymerases were compared in order to reveal differences in the properties of these enzymes responsible for the aphidicolin resistance of the mutant cell lines. Pol alpha's of the mutant cells show: (1) in vitro aphidicolin-resistance, (2) 1.5-3-fold lower specific activity than that of the wild type, (3) resistance to cytosine and adenosine arabinofuranoside 5'-triphosphate (araCTP and araATP), (4) altered resistance to carbonyldiphosphonate (COMDP) and to alkylphenyl nucleotide analogs (butylphenyl-dGTP and butylanilino-dATP), and (5) lower activity on poly(dA)/oligo(dT) template-primers. These changes in the biochemical properties of this enzyme may result from a mutation in pol alpha gene. Pol epsilon and delta of the mutant cells did not differ from the wild type enzymes with respect to aphidicolin resistance. However, the specific activities of these mutant enzymes were much higher (1.5 to 8-fold for pol epsilon and 4 to 20-fold for pol delta) in comparison to that of the wild type enzymes. Also in comparison to the wild type enzymes, the mutant pol epsilon showed changes in the template-primer preference; whereas the mutant pol delta was found to have altered sensitivity to other inhibitors. These results indicate that pol epsilon and pol delta are also altered as a secondary effect of mutation in the aphidicolin-resistant cells. It is suggested that these altered properties of the DNA pols of the alpha family are responsible for the in vivo aphidicolin resistance of the mutant cells.

Recombination by sequence repeats with formation of suppressive or residual mitochondrial DNA in Neurospora.

Recombination junctions of several Neurospora mitochondrial DNA (mtDNA) mutants and their revertants were identified. Their nucleotide sequences and putative secondary structures were determined in order to understand the nature of the elements involved in intramolecular recombination. Multiple deletions, involving the same portion of Neurospora mtDNA, were identified in six independently isolated mutants. A 9-nucleotide repeat element, CCCCNCCCC, was found to be involved in these and other Neurospora mitochondrial recombination events. The repeat elements were clustered as hot spots on the Neurospora mtDNA and were associated with palindromic DNA sequences. The palindromes have a potential to generate hairpin structures. A much lower free energy of the putative hairpins at the 5' end of the recombination site, and the possible formation of non-B-DNA structure by polypyrimidine tracks, may be important in the initiation of recombination. Using PCR, we found low levels of a specific mitochondrial deletion in certain Neurospora mutants. Their presence in low amounts in a population with a much larger number of normal mtDNA is unexpected. Contrary to earlier belief, this finding supports the view that deleted, smaller DNA molecules are not always suppressive relative to normal mtDNAs.

Characterization of a novel plasmid-like element in Neurospora crassa derived mostly from the mitochondrial DNA.

We have identified a plasmid-like element within mitochondria of Neurospora crassa strain stp-B1. It is derived from the EcoRI-4 and EcoRI-6 regions of the mitochondrial DNA, and an additional 124 bp DNA segment of unknown origin. The plasmid DNA consists of an oligomeric series of circular molecules of monomer length 2.2 kbp. The abundance of the plasmid suggests its autonomous replication and the presence of an efficient origin of replication. An unusually large number of palindromes capable of forming secondary structures are present in the plasmid. Such a palindrome, located near sequences reminiscent of mammalian and fungal mtDNA origins of replication, may define the replication origin of the plasmid. This putative origin might also represent the replication origin of the wild-type mtDNA.

Biochemical, genetic and ultrastructural defects in a mitochondrial mutant (ER-3) of Neurospora crassa with senescence phenotype.

The structural and functional abnormalities in a new respiratory deficient, mitochondrial senescence mutant ER-3 of Neurospora crassa are described. The mitochondrial mutant, which grows at a rate of only 10% of that of the wild type, was found deficient in all three cytochromes, and completely lacking in cytochromes aa3. Cytochrome oxidase activity in the mutant mitochondria was only about 5% of the wild type mitochondria. However, the total whole cell respiration rate of the mutant was 33% greater than that of the wild type, while the cyanide-resistant respiration rates were equal. The results of inhibitor studies clearly demonstrate that the mutant possesses a defect in one or more components of the terminal oxidase. Electron microscopic examination of whole cell sections and subsequent morphometric analysis revealed a significant (33%) reduction in membrane surface density of mitochondrial cristae in the mutant as compared with the wild type. Results of genetic and heterokaryon analyses indicate the location of mutation (ER-3) in the mitochondrial DNA. It is concluded that the senescence mutant ER-3 possesses a defect in the terminal portion of the mitochondrial respiratory apparatus. These results are consistent with previous analyses of mitochondrial DNA populations, and support the notion that obligately aerobic eukaryotic cells deficient in mitochondrial respiration necessarily exist as a result of stable heteroplasmosis and that defects in mitochondria lead to senescence in Neurospora mutant ER-3.