67 research outputs found

    Toxic metals (Cd and Pb) induced dysfunctioning of antioxidant system in marine fish Sphyraena barracuda (Edwards, 1771) collected from Kpeme, South of Togo

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    44-51Pollution of aquatic systems has become a recurring problem nowadays. The main goal of this study is to assess the impact of Cd and Pb on the antioxidant system of Sphyraena barracuda collected at Kpeme of South Togo. Two enzymatic biomarkers (catalase and glutathione-S-transferase) and two non-enzymatic biomarkers (malondialdehyde and glutathione) of oxidative stress were measured in various organs like liver, heart, gills and kidney of Sphyraena barracuda. The results indicated that stress was induced by Cd and Pb in these organs through lipid peroxidation and glutathione production. However, there was an alteration of the antioxidant system by low glutathione-S-transferase and catalase activities in the gills. Whereas, in other organs like heart, liver, and kidney, higher activity of glutathione-S-transferase and lesser activity of catalase was observed. From the results, it is very clear that Cd and Pb altered the antioxidant system of fish in comparison to the control samples

    Caracterización de los sistemas de captación de zinc y de hierro en Streptococcus suis : potencial antigénico y protector

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    Consultable des del TDXTítol obtingut de la portada digitalitzadaStreptococcus suis es un importante patógeno que causa grandes pérdidas económicas en la industria porcina a nivel mundial, siendo también un importante agente zoonótico. Aunque son varias las aproximaciones que se han desarrollado mediante vacunas vivas o recombinantes para prevenir las enfermedades provocadas por S. suis, los esfuerzos para controlar su infección se ven dificultados por la falta de herramientas efectivas contra este patógeno. Diferentes tipos de transportadores implicados en la captación de cationes divalentes y asociados a la pared celular, entre ellos los transportadores ABC, se relacionan con la virulencia bacteriana y presentan propiedades inmunogénicas contra las especies bacterianas de las que derivan. Atendiendo a todas estas características, se han desarrollado estrategias para producir vacunas contra las bacterias patógenas basadas en la sobreexpresión en la superficie celular bacteriana de transportadores de cationes divalentes inducidos mediante agentes quelantes o a través de la construcción de cepas deficientes en los represores de la transcripción de estos transportadores. En este contexto, el objetivo del presente trabajo ha sido estudiar los mecanismos de captación de cationes divalentes de S. suis, así como su papel en la virulencia y su posible uso para el desarrollo de herramientas eficaces contra este patógeno. Para abordar el objetivo propuesto, se identificaron in silico diversos transportadores de S. suis implicados en la captación de zinc y hierro y también sus posibles reguladores (AdcR y Fur, respectivamente). Además, se clonó el gen adcR de S. suis, que codifica un posible regulador de los transportadores implicados en la captación de Zn2+ y/o Mn2+ en Streptococcus spp., se purificó la proteína AdcR y mediante ensayos con DNasaI (footprinting) y de movilidad electroforética se demostró, por primera vez, que dicha proteína reconoce y se une específicamente a la secuencia TTAACNRGTTAA. Asimismo, también se ha demostrado que in vitro se requiere Zn2+ o Mn2+ para establecer dicha unión y que la proteína AdcR controla la expresión de los genes que codifican las proteínas SsuiDRAFT 0103 y SsuiDRAFT 1237, componentes de transportadores ABC implicados en la captación de zinc y/o manganeso. Por otra parte, se clonó el gen fur de S. suis, que codifica el posible regulador de los transportadores implicados en la captación de Fe2+, y se sobreexpresó su producto en Escherichia coli. Ensayos de movilidad electroforética con extracto crudo de esta cepa de E. coli mostraron que la proteína Fur de S. suis controla la expresión de los genes feoAB, implicados en la captación de hierro. Seguidamente, se obtuvieron mutantes mediante la deleción de los genes adcR y fur en una cepa virulenta de S. suis con el objetivo de caracterizar ambos regulones. Varios transportadores implicados en la captación de cationes aparecieron desreprimidos en las cepas mutantes cuando la expresión génica fue comparada con la de la cepa salvaje a través de ensayos de RT-PCR a tiempo real. En concordancia con ello, los ensayos de movilidad electroforética mostraron que estos reguladores se unen específicamente al promotor de dichos genes. Asimismo, la ausencia de los genes adcR y/o fur en un estreptococo patógeno mostró, por primera vez, una importante atenuación de su virulencia en el modelo animal de ratón. Finalmente, se abordaron estudios de inmunogenicidad y protección. Para ello, se purificaron tres proteínas periplásmicas de S. suis implicadas en la captación de cationes divalentes (SsuiDRAFT 0103, SsuiDRAFT 0174 y SsuiDRAFT 1237), resultando ser todas ellas inmunogénicas, aunque sólo SsuiDRAFT 0103 confiere una protección significativa contra S. suis en el modelo animal de ratón. Además, las proteínas Ssu0309 y Ssu1103 asociadas a la pared celular, que están sobreexpresadas en el mutante adcR, fueron identificadas mediante espectrometría de masas como factores de virulencia pertenecientes a la familia de proteínas Pht (Pneumococcal histidine triad). Asimismo, se estudiaron las propiedades protectoras de las cepas mutantes demostrándose que aunque enteras no confieren protección contra S. suis en el modelo animal de ratón, las proteínas asociadas a la pared celular del doble mutante adcR fur sí que inducen una protección significativa ante una infección con la cepa virulenta de S. suis 89/1591 en dicho modelo.Streptococcus suis is an important pathogen that causes significant economical losses in the swine industry worldwide and it is also an important zoonotic agent. Although several approaches to develop either live or recombinant vaccines to prevent S. suis-mediated disease have been tested, efforts to control the infection are hampered by the lack of effective weapons against this pathogen. Different cell-wall-associated transporters involved in divalent-cation uptake, including ABC transporters, have been shown to be involved in bacterial virulence and have immunogenic properties against the bacterial species from which they are derived. Accordingly, several strategies have been developed to produce vaccines against this pathogenic bacterium. One of them involves overexpression on the bacterial cell surface of divalent-cation-uptake transporters induced by chelator agents or by the construction of deficient strains in the cation-uptake repressors. In this context, the aim of this work has been to study the S. suis-cation-uptake mechanisms and their role in virulence as well as their putative use as a tool to achieve broad protection against this pathogen. To achieve this purpose, several transporters involved in zinc and iron uptake and their putative regulators (AdcR and Fur, respectively) have been identified in silico. Furthermore, the S. suis adcR gene, which encodes a predicted regulator of Zn2+ and/or Mn2+ uptake in streptococci, was cloned and its protein product was purified. Footprinting and electrophoretic mobility shift assays with purified S. suis AdcR protein showed, for the first time, that the AdcR-DNA binding sequence corresponds to the TTAACNRGTTAA motif. In addition, the requirement for either Zn2+ or Mn2+ to establish in vitro binding of AdcR to its target sequence and the ability of AdcR to control the genes codifying the ABC-transporter components SsuiDRAFT 0103 and SsuiDRAFT 1237, involved in zinc and/or manganese uptake, were demonstrated. Besides, the S. suis fur gene, which encodes a predicted regulator of Fe2+ uptake, was cloned and its protein product was overexpressed in Escherichia coli. Electrophoretic mobility shift assays with crude extract of this E. coli strain showed that S. suis Fur protein controls the feoAB genes, involved in ferric uptake. In addition, both adcR and fur genes were deleted in a virulent S. suis strain in order to charecterize these regulons. Several cation-uptake transporters appeared desrepressed in the knockout strains when gene expression was compared with wild-type strain through real-time RT-PCR analyses. Accordingly, EMSA results showed that these regulators specifically bind to the promoter of these genes. Moreover, the absence of adcR and/or fur genes in pathogenic streptococci showed, for the first time, an important attenuation of its virulence in mice. Finally, immunogenic and protective analysis were carried out with the products of three genes encoding putative divalent-cation-binding lipoproteins of S. suis (SsuiDRAFT 0103, SsuiDRAFT 0174, and SsuiDRAFT 1237), being all of them immunogenic although only one (SsuiDRAFT 0103) induces a significant protective response against a virulent S. suis strain in mice. Moreover, the overexpressed cell wall-associated proteins Ssu0309 and Ssu1103 of the adcR mutant, were identified by mass spectrometry as putative virulence factors belonging to the Pht (Pneumococcal histidine triad) family. Likewise, protective abilities of mutant strains were analyzed showing that although mutant cells are not effective to confer protection in mice, the combination of adcR- and fur-regulated cell wall-associated proteins confers a significant protection against S. suis 89/1591 challenge to mice vaccinated with them

    Idiops joida Gupta, Das and Siliwal, sp. nov.

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    Idiops joida Gupta, Das and Siliwal sp. nov. (Figs 1 A – L, 2 A – F, Table 1) Type specimens. Holotype male. INDIA: Karnataka: Uttara Kannada, Joida [15 ° 11 ' 36.1314 "N, 74 ° 29 ' 36.528 "E], 12 April 2010, elev. 609 m, coll. N. Gupta, S. Chauhan and Ramesh (WILD- 10 -ARA- 913). Paratypes. INDIA: Karnataka: 2 females, same data as holotype (WILD- 10 -ARA- 914, WILD- 10 -ARA- 909); 2 females, same data as holotype, 26 March 2010 (WILD- 10 -ARA- 803, WILD- 10 -ARA- 805). Diagnosis. Males of Idiops joida sp. nov. closely resemble those of I. garoensis and I. pylorus in having a stout spine on the tibial spur of leg I (Fig. 1 F) but males can be distinguished from those of other Idiops species by having metatarsi I slender and lacking the prolateral process; males differ from those of I. garoensis by the leg formula 4123 (In I. garoensis, leg formula 1432); they also differ from those of I. pylorus also by having ocular area distinctly longer than wide (in I. pylorus, the ocular area is slightly wider than long). Females of Idiops joida sp. nov. resemble those of I. constructor, I. fortis and I. oriya in having a band of spinules on coxae IV but differ from them in having tibia III distinctly longer than wide and leg formula 4132 (I. constructor and I. fortis, leg I and leg IV subsequal in length and tibia III is as long as wide; I. oriya, tibia III slightly longer than wide and leg II is longer than leg III). Etymology. The species epithet is a name in apposition from the type locality, Joida, in Uttara Kannada, Karnataka. Description. Holotype Male: Total length 10.86. Carapace 4.71 long, 4.12 wide; chelicerae 2.57 long; abdomen 6.15 long, 4.06 wide. Spinnerets: PMS, tuft 0.33 long, 0.12 wide, 0.21 apart; PLS, 0.56 basal, 0.23 middle, 0.35 distal; midwidths 0.67, 0.49, 0.26 respectively; 1.14 total length. LEG I LEGII continued. continued. PALP HT*= Holotype, PT= Paratypes. Colour in life. Carapace, chelicerae blackish-brown. Legs and palp black except for tarsi of all legs and palp, mt II–III distal 3 / 4 th, mt I distal ½, mt IV and tibia of palp pale yellowish-brown. Abdomen dorsally uniformly grayish-black, ventrally and ventro-laterally uneven shades of grayish-brown. Spinnerets brown. Colour in alcohol. Carapace, chelicerae greenish-brown. Legs greenish-brown except for tarsi of all legs and palp, mt II–III distal 3 / 4 th, mt I distal ½, mt IV and tibia of palp yellow. Abdomen dorsally grayish-brown with faint pale spots radiating in curved lines; ventrally and ventro-laterally uneven shades of yellowish-gray. Spinnerets yellowish-brown. Carapace (Fig. 1 A). Oval, wart-like tubercles except for striae and around eyes, less conspicuous in anterior caput. Fovea procurved, deep. Bristles absent. Eyes (Figs 1 A–B). Eight in three rows, ALE situated far from AME on clypeal edge; posterior row procurved. Ocular group 0.96 long, 0.95 wide; MOQ not square, 0.57 front width and 0.52 back width, 0.51 long. Diameter AME 0.15, PME 0.14, ALE 0.18, PLE 0.17; distance between ALE-AME 0.28, AME-AME 0.02, PLE-PME 0.02, PME-PME 0.13, ALE-PLE 0.50, ALE-ALE adjacent. Maxillae (Fig. 1 C). 2.13 long anteriorly, 2.60 long posteriorly, 1.47 wide; no cuspules; anterior lobe distinct, posterior edge obscured, anterior edge straight. Labium (Fig. 1 C). 0.54 long, 0.96 wide, labiosternal groove shallow, slightly procurved with no cuspules. Chelicerae (Figs 1 C–D). 9 teeth on promarginal and 6 teeth on retromarginal; depression on retrolateral face where fang touches chelicerae; rastellum strong, raised on high triangular mound, with 13 thick, short spines, surrounded with many normal spines; two glabrous bands for length of dorsal surface of chelicerae. Sternum (Fig. 1 C). 2.66 long, 2.35 wide, broader between posterior coxae; yellowish-brown, elevated in centre, sloping laterally, covered with short and long black bristles; row of long bristles on margins, posterior angle acute. Sigilla (Fig. 1 C). Posterior sigilla absent; median pair marginal, 1.68 apart, 0.07 from margin and anterior pair round, marginal. Legs. All legs cylindrical, not flattened; leg I thicker than II–IV; femora III clearly wider than rest; metatarsi of all legs longer than tarsi. Tibia I inflated with two distal, prolateral tibial spurs with spines, anterior spur facing upward (at about 45 o) with curved, stout spine, below small spine on tubercle facing diagonally opposite to anterior spur (Figs 1 E–F); mt I cylindrical, not incrassate, gently curved retrolaterally (Fig. 1 E). Legs covered with few scattered hair, bristles and normal pointed spines. Two conspicuous glabrous bands for length of femora, patellae and tibiae. Leg formula 4123. Scopulae. Ta I, few scopuliform hair in distal half; ta II–III well developed, distal 3 / 4 th; ta IV, rudimentary, almost absent. Spines. More on promarginal and retromarginal sides of legs and palp. I: ti, p= 2 spur with megaspine, r= 6; mt, p= 1, r= 6; ta, p= 1, r= 3. II: ti, r= 2; mt, p= 2, r= 6; ta, r= 3. III: fe, p= 2; pa, p= 10,r= 3; ti, p= 7, r= 4; mt, p= 5, v= 9, r= 4; ta, p= 3, r= 4. IV: pa, p= 9; ti, p= 1, v= 3, r= 1; mt, p= 1, v= 6, r= 1; ta, p= 3, v= 6, r= 3. Palp: ti, r= 39; ta, d= 3. Trichobothria. Clavate absent; ta I, 13 long filiform for length; ta II, 10 long filiform for length; ta III, 16 long filiform in basal two thirds; ta IV, 9 long filiform and 7 long filiform on palp in centre, all trichobothria in two zigzag rows. Mt I, 5 long filiform in distal one thirds; mt II–IV, 6 long filiform in distal one thirds. Leg coxae. Greenish-yellow, covered with short and long black bristles. Coxae IV with short spinule-like bristles in anterior half, rest sparsely covered with long bristles. Claws (Figs 1 G–H). All legs with paired and unpaired claws. Both (paired as well as unpaired) claws on IV prominent and larger than I–III. Paired claws with four teeth on leg I, 2 + 1 bifid tooth on leg II, 1 + 1 bifid tooth on leg III, three unequal sized teeth on leg IV. False claw tufts on either sides of paired claws. Abdomen (Fig. 1 A). Covered with short black hair with few long bristle-like hairs posteriorly, cuticle appears leathery and slightly rough. Ventrally uniformly covered with short and few long black hairs. Spinnerets (Fig. 1 I). PMS digitiform covered with brown hair; PLS covered with brown hair, apical segment domed. Palp (Figs 1 J–L). Tibia inflated, ventral 1 / 3 rd incrassate with band of spines on retrolateral side of cavity. Cymbium truncated dorsally with two lateral processes. Median haematodocha fused with bulb, embolus tapering and curved 45 o at tip, slightly flattened just before tip. Description. Female (WILD- 10 -ARA- 914): Total length 14.00. Carapace 5.15 long, 4.76 wide; 3.76 long chelicerae; abdomen 8.85 long, 5.51 wide. Spinnerets: PMS, 0.41 long, 0.14 wide, 0.21 apart; PLS, 0.85 basal, 0.47 middle, 0.32 distal; midwidths 1.11, 0.95, 0.57 respectively; 1.64 total length. Colour in life. Carapace and chelicerae, blackish-brown. Legs reddish-brown above and light yellowish green below, except tarsi of palp and metatarsi and tarsi of all legs blackish-brown above and brown below; abdomen dorsally grayish-brown mid-dorsally and gradually lighter brown laterally, ventrally creamish-brown. Spinnerets yellowish-brown. Colour in alcohol. Carapace, chelicerae, reddish-brown. Legs and palp yellowish-brown, lighter below. Abdomen dorsally greenish-brown, ventrally yellowish-brown. Spinnerets yellowish-brown. Carapace (Fig. 2 A). Glabrous, broader anteriorly (widest between legs II) and gradually narrowing posteriorly, striae prominent. Fovea, procurved, deep. Bristles: 2 long and several short on caput; 1 long and three short on clypeus edge. Eyes (Figs 2 A–B). Eight in three rows, ALE situated far from AME on clypeal edge; posterior row procurved. Ocular group 1.28 long, 1.22 wide; MOQ square, 0.63 wide, 0.56 long. Diameter AME 0.18, PME 0.21, ALE 0.26, PLE 0.25; distance between ALE-AME 0.42, AME-AME 0.05, PLE-PME 0.08, PME-PME 0.16, ALE-PLE 0.67, ALE-ALE adjacent. Maxillae (Fig. 2 C). 1.01 long anteriorly, 1.29 long posteriorly, 1.74 wide; 70 cuspules; anterior lobe distinct. Labium (Fig. 2 C). 0.90 long, 1.07 wide, labiosternal groove shallow, slightly procurved with 13 cuspules. Chelicerae (Figs 2 C–D). 7 teeth on promarginal and 8 teeth on retromarginal; depression on retrolateral face where fang touches chelicerae; rastellum strong, raised on high triangular mound, with 16 thick, short spines, surrounded by many normal long spines; two glabrous bands for length of dorsal surface of chelicerae. Sternum (Fig. 2 C). 3.18 long, 2.96 wide, broader between posterior coxae; yellowish-brown, elevated in centre, sloping laterally, covered with long black bristles; row of long bristles on margins, posterior angle acute. Sigilla (Fig. 2 C). Posterior sigilla absent; median pair submarginal, 2.05 apart, 0.10 from margin and anterior pair round, marginal. Legs. Femora and tibiae III wider than others; all metatarsi longer than respective tarsi. Tibiae, metatarsi and tarsi of legs I–II and tibiae and tarsi of palp dorsoventrally flattened, other legs normal. Legs covered with few scattered hair, bristles and few curved thick thorn-like spines. Two conspicuous glabrous bands for length of femora, patellae and tibiae. Scopulae absent on tarsi of all legs and palp. Leg formula 4132. Spines. More on promarginal and retromarginal sides of legs and palp. I: pa, v= 1, r= 1; ti, p= 14, r= 16; mt, p= 19, r= 16; ta, p= 7, r= 11, v= 3. II: fe, d= 1; pa, p= 1; ti, p= 3, r= 17; mt, p= 15, r= 16; ta, p= 7, r= 11, v= 1. III: pa, p= 1; ti, p= 9, r= 4; mt, p= 14, r= 10; ta, p= 9, r= 4. IV: ti, v= 2; mt, p= 5, r= 1, v= 3; ta, p= 11, r= 4. Palp: fe, p= 1, r= 2; pa, r= 1; ti, p= 18, r= 16; ta, p= 21, r= 24, v= 2. Trichobothria. Clavate absent; ta I, 12 long filiform in each of four rows for length; ta II, 14 long filiform in 2 rows for length; ta III, 18 long filiform in basal two thirds; ta IV, 9 long filiform and 12 long filiform in two rows on palp. Mt I, 5 long filiform in distal fourth; mt II–IV, 7 long filiform in distal fourth. Leg coxae. Yellowish-brown, covered with short and long black bristles. Coxa III with central patch without hair or spinules, others sparsely covered with long bristles; coxa IV clearly broader than others, anterior edge curved, ventrally, broad patch of spinules in distal 3 / 4 th, others covered with long bristles. Claws. All legs with paired and unpaired claws. Both (paired as well as unpaired) claws on leg IV prominent and larger than on other legs. Paired claws with 2 unequal size teeth on legs I, III– IV; 1 tooth on leg II; bifid tooth on palp. False claw tufts on each side of paired claws. Abdomen (Fig. 2 A). Oval, uniformly covered with short and long black hairs. Dorsum with few black patches, cuticle appears leathery and slightly rough. Spinnerets (Fig. 2 E). PMS digitiform covered with brown hair; PLS covered with brown hair, apical segment domed. Spermathecae (Fig. 2 F). Two single lobes facing away from each other; each lobe, resembles ice-cream on cone, with distal 2 / 3 rd bulged and curved dorsal and lateral edges, covered with pores, otherwise lobes sclerotized, gradually narrowing (cone shape) and opens ventrally; transparent sheet of inverted triangular shape covers basal half of sclerotized lobes. Variation. Females: Total length 14–18.44 (16.22 ± 2.36). Carapace: 5.15–7.99 (6.66 ± 1.20) long, 4.76–6.35 (5.70 ± 0.71) wide; MOQ: 0.56–0.74 (0.67 ± 0.08) long, front width 0.63–0.74 (0.70 ± 0.05), back width 0.63–0.84 (0.76 ± 0.09). Difference between front width and back width: 0.00– 0.11 (0.06 ± 0.05). Labium: 0.90–1.47 (1.20 ± 0.23) long, 1.07–1.43 (1.27 ± 0.17) wide; cuspules 6–14. Maxillae: 1.01–1.43 (1.23 ± 0.17) long in front, 1.29–1.43 (1.35 ± 0.07) long in back, 1.74–2.47 (2.20 ± 0.33) wide; cuspules 70–130 (90). Sternum: 3.18–4.57 (3.89 ± 0.62) long, 2.96–3.99 (3.55 ± 0.46) wide. Abdomen: 8.00– 11.32 (9.57 ± 1.45) long, 5.35–8.17 (6.68 ± 1.46) wide. Spinnerets: PLS, 0.77–0.92 (0.86 ± 0.07) basal, 0.31–0.55 (0.44 ± 0.10) middle, 0.26–0.32 (0.29 ± 0.03) apical; midwidths, 1.00– 1.11 (1.05 ± 0.05), 0.76–0.95 (0.85 ± 0.08), 0.47–0.67 (0.57 ± 0.08) respectively; 1.34–1.73 (1.59 ± 0.17) total length; PMS, 0.41–0.79 (0.60 ± 0.16) long, 0.14–0.28 (0.24 ± 0.07) wide; distance between PMS–PMS, 0.21–0.54 (0.36 ± 0.14). Natural history. I. joida was found in almost every habitat surveyed, including semi-evergreen, moist deciduous, agriculture, teak plantations and human habitations. It certainly preferred open and exposed microhabitats, like human settlements and agriculture over the closed and unexposed ones, like semi-evergreen. The burrows were located in March–April and all active burrows were mostly found occupied by adult and/or nesting females, juveniles and sub-adults. Males are usually wanderers and difficult to locate in burrows (Siliwal, 2009), and therefore only one sub-adult spider was found and collected from its burrow; it later moulted to a male in the vial. The burrows occurred on steep (90 °) as well as gentle slopes (45 °), and horizontal (less than 10 °), and occupied various substrates like vertical bunds, soil deposits at the base of tree trunks, flat ground and occasionally observed on termite hills. The burrows were simple tube-like with a ‘D’-shaped trapdoor of variable thickness. Further, all excavated burrows were observed to have one of the three types of shapes: straight, gently curved and C-shape. The burrow diameter ranged from 2 to 18mm and the depth of burrows ranged from 10 to 185mm. The burrow diameter was found to be almost constant throughout the descending depth of the burrow. But burrows of most gravid or nesting females were wider at the bottom. When a burrow was disturbed, the spider retreated at the bottom of the burrow and, if nesting, went deep inside the burrow holding the egg-sac and remained there until the burrow was fully excavated. Similar behaviour has been reported in many other members of barychelids and idiopids (Raven, 1994). The egg-sacs consisted of 50– 250 eggs bound together in thick silk lining.Published as part of Gupta, Neha, Ganeshkumar, M., Das, Sanjay Keshari & Siliwal, Manju, 2013, Three new species of Idiops Perty, 1833 (Araneae: Idiopidae) from India, pp. 237-250 in Zootaxa 3635 (3) on pages 239-244, DOI: 10.11646/zootaxa.3635.3.3, http://zenodo.org/record/21603

    A Supervised Machine Learning Model for Tool Condition Monitoring in Smart Manufacturing

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    In the current industry 4.0 scenario, good quality cutting tools result in a good surface finish, minimum vibrations, low power consumption, and reduction of machining time. Monitoring tool wear plays a crucial role in manufacturing quality components. In addition to tool monitoring, wear prediction assists the manufacturing systems in making tool-changing decisions. This paper introduces an industrial use case supervised machine learning model to predict the turning tool wear. Cutting forces, the surface roughness of a specimen, and flank wear of tool insert are measured for corresponding spindle speed, feed rate, and depth of cut. Those turning test datasets are applied in machine learning for tool wear predictions. The test was conducted using SNMG TiN Coated Silicon Carbide tool insert in turning of EN8 steel specimen. The dataset of cutting forces, surface finish, and flank wear is extracted from 200 turning tests with varied spindle speed, feed rate, and depth of cut. Random forest regression, Support vector regression, K Nearest Neighbour regression machine learning algorithms are used to predict the tool wear. R squared, the technique shows the random forest machine learning model predicts the tool wear of 91.82% of accuracy validated with the experimental trials. The experimental results exhibit flank wear is mainly influenced by the feed rate followed by the spindle speed and depth of cut. The reduction of flank wear with a lower feed rate can be achieved with a good surface finish of the workpiece. The proposed model may be helpful in tool wear prediction and making tool-changing decisions, which leads to achieving good quality machined components. Moreover, the machine learning model is adaptable for industry 4.0 and cloud environments for intelligent manufacturing systems

    Digital Twin Framework for Lathe Tool Condition Monitoring in Machining of Aluminium 5052

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    Digital Twin (DT) is a virtual representation of a product system that exhibits the properties and analyzes the system’s functions. The significant impact of DT extends to several fields, which increases productivity and reduces wastage. This article focuses on developing a Digital twin model of a Lathe machine for Tool Condition Monitoring (TCM). DT implementation in industries is challenging due to simulating online cutting forces and wear. Even though several pieces of research have been carried out in the prediction of tool conditions using machine learning, Artificial Neural network models, only a few pieces of research have been made in digital twins for TCM. This article provides the technique for implementing the DT model of a lathe tool. The feasibility of the DT Model framework is verified by a case study of the turning process with a CNC Lathe machine while machining of Aluminium 5052 workpiece using Titanium Nitride coated tool inserts. The sensor’s data are acquired and fed to the microcontroller for real-time data acquisition. The real-time dataset is processed in the DT model for monitoring and predicting the tool conditions. The tool wear classification using the DT model is achieved. Developing the Digital Twin model in machining increases productivity and assists in predictive maintenance

    The DeoR-type transcriptional regulator SugR acts as a repressor for genes encoding the phosphoenolpyruvate: sugar phosphotransferase system (PTS) in Corynebacterium glutamicum

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    Gaigalat L, Schlüter J-P, Hartmann M, et al. The DeoR-type transcriptional regulator SugR acts as a repressor for genes encoding the phosphoenolpyruvate: sugar phosphotransferase system (PTS) in Corynebacterium glutamicum. BMC Molecular Biology. 2007;8(1): 104.Background: The major uptake system responsible for the transport of fructose, glucose, and sucrose in Corynebacterium glutamicum ATCC 13032 is the phosphoenolpyruvate:sugar phosphotransferase system (PTS). The genes encoding PTS components, namely ptsI, ptsH, and ptsF belong to the fructose-PTS gene cluster, whereas ptsG and ptsS are located in two separate regions of the C. glutamicum genome. Due to the localization within and adjacent to the fructose-PTS gene cluster, two genes coding for DeoR-type transcriptional regulators, cg2118 and sugR, are putative candidates involved in the transcriptional regulation of the fructose-PTS cluster genes. Results: Four transcripts of the extended fructose-PTS gene cluster that comprise the genes sugR-cg2116, ptsI, cg2118-fruK-ptsF, and ptsH, respectively, were characterized. In addition, it was shown that transcription of the fructose-PTS gene cluster is enhanced during growth on glucose or fructose when compared to acetate. Subsequently, the two genes sugR and cg2118 encoding for DeoR-type regulators were mutated and PTS gene transcription was found to be strongly enhanced in the presence of acetate only in the sugR deletion mutant. The SugR regulon was further characterized by microarray hybridizations using the sugR mutant and its parental strain, revealing that also the PTS genes ptsG and ptsS belong to this regulon. Binding of purified SugR repressor protein to a 21 bp sequence identified the SugR binding site as an AC-rich motif. The two experimentally identified SugR binding sites in the fructose-PTS gene cluster are located within or downstream of the mapped promoters, typical for transcriptional repressors. Effector studies using electrophoretic mobility shift assays (EMSA) revealed the fructose PTS-specific metabolite fructose-1-phosphate (F-1-P) as a highly efficient, negative effector of the SugR repressor, acting in the micromolar range. Beside F-1-P, other sugar-phosphates like fructose-1,6-bisphosphate (F-1,6-P) and glucose-6-phosphate (G-6-P) also negatively affect SugR-binding, but in millimolar concentrations. Conclusion: In C. glutamicum ATCC 13032 the DeoR-type regulator SugR acts as a pleiotropic transcriptional repressor of all described PTS genes. Thus, in contrast to most DeoR-type repressors described, SugR is able to act also on the transcription of the distantly located genes ptsG and ptsS of C. glutamicum. Transcriptional repression of the fructose-PTS gene cluster is observed during growth on acetate and transcription is derepressed in the presence of the PTS sugars glucose and fructose. This derepression of the fructose-PTS gene cluster is mainly modulated by the negative effector F-1-P, but reduced sensitivity to the other effectors, F-1,6-P or G-6-P might cause differential transcriptional regulation of genes of the general part of the PTS (ptsI, ptsH) and associated genes encoding sugar-specific functions (ptsF, ptsG, ptsS)
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