IKK inhibitor PubMedCrossRef 10. Gilleland HE Jr, Parker MG, Matthews JM, Berg RD: Use of a purified outer membrane protein F (porin) preparation of Pseudomonas aeruginosa as a SB-715992 manufacturer protective vaccine in mice. Infect Immun 1984, 44:49–54.PubMed 11. Gilleland HE Jr, Gilleland LB, Matthews-Greer JM: Outer membrane protein F preparation of Pseudomonas aeruginosa as a vaccine against chronic pulmonary infection with heterologous immunotype strains in a rat model. Infect Immun 1988, 56:1017–1022.PubMed 12. von Specht BU, Lucking HC, Blum B, Schmitt A, Hungerer KD, Domdey H: Safety and

immunogenicity of a Pseudomonas aeruginosa outer membrane protein I vaccine in human volunteers. Vaccine 1996, 14:1111–1117.PubMedCrossRef 13. Gilleland HE, Gilleland LB, Staczek J, Harty RN, Garcia-Sastre A, Palese P, Brennan FR, Hamilton WD, Bendahmane FK228 M, Beachy RN: Chimeric animal and plant viruses expressing epitopes of outer membrane protein F as a combined vaccine against Pseudomonas aeruginosa lung infection. FEMS Immunol Med Microbiol 2000, 27:291–297.PubMedCrossRef 14. Battershill JL, Speert DP, Hancock RE: Use of monoclonal antibodies to protein F of Pseudomonas aeruginosa as opsonins for phagocytosis by macrophages. Infect Immun 1987, 55:2531–2533.PubMed 15. Lee NG, Ahn BY, Jung SB, Kim YG, Lee Y, Kim HS, Park WJ: Human anti- Pseudomonas aeruginosa

outer membrane proteins IgG cross-protective against infection with heterologous immunotype strains of P. aeruginosa . FEMS Immunol Med Microbiol 1999, 25:339–347.PubMed 16. Baumann U, Mansouri E, von Specht BU: Recombinant OprF-OprI as a vaccine against Pseudomonas aeruginosa infections. Vaccine 2004, 22:840–847.PubMedCrossRef 17. PAK5 Hughes EE, Gilleland HE Jr: Ability of synthetic peptides representing epitopes of outer membrane protein F of Pseudomonas aeruginosa to afford protection against P. aeruginosa infection in a murine acute pneumonia model. Vaccine 1995, 13:1750–1753.PubMedCrossRef 18. Worgall S, Kikuchi T, Singh R, Martushova K, Lande L, Crystal RG: Protection against pulmonary infection with Pseudomonas aeruginosa

following immunization with P. aeruginosa -pulsed dendritic cells. Infect Immun 2001, 69:4521–4527.PubMedCrossRef 19. Tacken PJ, de Vries IJ, Torensma R, Figdor CG: Dendritic-cell immunotherapy: from ex vivo loading to in vivo targeting. Nat Rev Immunol 2007, 7:790–802.PubMedCrossRef 20. Fajardo-Moser M, Berzel S, Moll H: Mechanisms of dendritic cell-based vaccination against infection. Int J Med Microbiol 2008, 298:11–20.PubMedCrossRef 21. Steinman RM, Banchereau J: Taking dendritic cells into medicine. Nature 2007, 449:419–426.PubMedCrossRef 22. Lopez-Bravo M, Ardavin C: In vivo induction of immune responses to pathogens by conventional dendritic cells. Immunity 2008, 29:343–351.PubMedCrossRef 23. Kikuchi T, Crystal RG: Antigen-pulsed dendritic cells expressing macrophage-derived chemokine elicit Th2 responses and promote specific humoral immunity. J Clin Invest 2001, 108:917–927.PubMed 24.

Ergonomics 47(1):1–18CrossRef Hughes RE, Silverstein BA, Evanoff

BA (1997) Risk factors for work-related musculoskeletal disorders in an aluminum smelter. Am J Ind Med 32:66–75CrossRef Kuijer PP, Hoozemans MJ, Kingma I et al (2003) Effect of a redesigned two-wheeled container for refuse collecting on mechanical loading of low back and shoulders. Ergonomics 46(6):543–560CrossRef STAT inhibitor Kuijer PP, Hoozemans MJ, Frings-Dresen MH (2007) A different approach for the ergonomic evaluation of pushing and pulling in practice. Int J Ind Ergo 37:855–862CrossRef Seidler A, Bolm-Audorff U, Petereit-Haack G et al. (2011) Work-related lesions of the supraspinatus tendon: a case-control study. Int Arch Occup Environ Health 84(4):425–433 Smedley J, Inskip H, Trevelyan F, Buckle P, Cooper C,

Coggon D (2003) Risk factors for incident neck and shoulder pain in hospital nurses. Occup Environ Med 60(11):864–869 Van der Beek AJ, Frings-Dresen MHW, Van Dijk FJH, Kemper HCG, Meijman TF (1993) selleck kinase inhibitor Loading and unloading by lorry drivers and musculoskeletal complaints. Int J Ind Ergo 12:13–23CrossRef”
“Introduction Health promotion is a cornerstone of public health policy in most western Entinostat cell line countries. In order to reach as many individuals as possible, different settings are explored to provide health promotion programs. Because of the possibility to reach large groups, and the presence of a natural social network, the workplace is regarded as a promising context for health promotion. The World Health Organization (WHO 2010a) has described the workplace as one of the priority settings for health promotion into the 21st century, and the World Health Assembly of the WHO (2010b) endorsed the “Workers’ health: Global Plan of Action”, aimed to protect and promote health at the workplace. Workplace health promotion (WHP) is defined as the combined efforts of employers, employees, and society to improve the health and wellbeing of people at work.

The European Agency for Safety and Health at Work else (2010) describes that WHP should be achieved by promoting the participation of workers in the whole process of WHP. Employers are encouraged to provide health promotion activities to their employees. With the aim to become the worlds’ healthiest country in 2020, Australia gives workplaces a key role in preventative health (Australian Government Preventive Health Taskforce 2008). Individual health risk assessments and health risk reduction programs aimed at lifestyle are popular applications for WHP (for example Ott et al. 2010; Rocha et al. 2010). However, the participation in such programs varies considerably between companies and is often low (Robroek et al. 2009).

6. Conclusions Physiological adaptations to physical exercises lead to blood volume redistribution favoring the working muscle supply with oxygen and energy-yielding substrate as well as the skin for heating dissipation as sweat. Strenuous exercise and/or hot-humid environments precipitate body dehydration, which may induce core hyperthermia, Pevonedistat muscle glycogen depletion, gastric emptying delay, gut underperfusion (and ischemia) followed by endotoxemia or anaphylaxis. Rapid fluid delivery from fluids intake is the goal of oral rehydration solutions and sports drinks, that provide the addition of sodium and carbohydrates to assist the intestinal

absorption of water and muscle-glycogen replenishment, respectively. However, sometimes, fluid delivery and carbohydrate delivery are difficult to reconcile as carbohydrate-rich beverages decrease fluid delivery to the gut, thus delaying water absorption and accentuating gut underperfusion. It is necessary to inform athletes about potential dangers of drinking too much water, advise them to refrain from using hypertonic fluid

replacements. Nutritional Recommendations During intense exercise, is recommended an intake of 0,5 L/hour TGF-beta family of sports beverages. A CHO (<10%) and sodium beverage should be encouraged. To increase the CHO exogenous oxidation, glucose plus fructose should be consumed. References 1. Burini FHP, de Oliveira EP, Burini RC: Metabolic

(Mal) Adaptations to Training Continuum-Misconceptions of Terminology and Diagnosis. Rev Bras Med Esporte 2010, 16:388–392.CrossRef 2. Wittbrodt ET: Maintaining fluid and Captisol electrolyte balance during exercise. Journal of Pharmacy Practice 2003, Sodium butyrate 16:45–50.CrossRef 3. de Oliveira EP, Burini RC: The impact of physical exercise on the gastrointestinal tract. Curr Opin Clin Nutr Metab Care 2009, 12:533–538.PubMedCrossRef 4. Choi JH, Lee HB, Ahn IS, Park CW, Lee CH: Wheat-dependent, Exercise-induced Anaphylaxis: A Successful Case of Prevention with Ketotifen. Ann Dermatol 2009, 21:203–205.PubMedCrossRef 5. Fujii H, Kambe N, Fujisawa A, Kohno K, Morita E, Miyachi Y: Food-dependent exercise-induced anaphylaxis induced by low dose aspirin therapy. Allergol Int 2008, 57:97–98.PubMedCrossRef 6. Rehrer NJ, Brouns F, Beckers EJ, Frey WO, Villiger B, Riddoch CJ, Menheere PP, Saris WH: Physiological changes and gastro-intestinal symptoms as a result of ultra-endurance running. Eur J Appl Physiol Occup Physiol 1992, 64:1–8.PubMedCrossRef 7. Qamar MI, Read AE: Effects of exercise on mesenteric blood flow in man. Gut 1987, 28:583–587.PubMedCrossRef 8. Jeukendrup AE, Jentjens RL, Moseley L: Nutritional considerations in triathlon. Sports Med 2005, 35:163–181.PubMedCrossRef 9.

Furthermore, to evaluate the potential of negative lamin A/C expression (negative vs. positive) as an independent predictor for overall survival of GC, multivariate Cox regression analyses were performed. While tumour invasion failed to demonstrate independency, only status of metastasis and negative lamin A/C expression may play a role to GS-1101 supplier predict the overall survival in GC (p = 0.040 and p = 0.041, respectively; Table 3). Table 3 The overall survival univariate and multivariate Cox regression analysis Clinicopathological Variable Relative Risk (95% CI) p -Value Univariate        Gender 0.948 (0.549–1.637) 0.038    Tumour Size 1.621 (0.974–2.697)

0.063    Metastasis find more Roscovitine clinical trial 2.057 (1.110–3.810) 0.022a    Invasion 2.012 (1.098–3.698) 0.024a    Stage 0.915 (0.709–1.181) 0.497    Histological Differentiation 1.704 (0.969–2.997) 0.064    Lamin A/C 0.582 (0.349–0.969) 0.038a Multivariate        Metastasis 1.905 (1.029–3.526) 0.040a    Lamin A/C 0.585 (0.350–0.978) 0.041a Abbreviation: 95% CI, 95% confidence interval. a Statistically significant (p < 0.05).

Figure 5 Estimated overall survival according to the expression of lamin A/C in 126 cases of GCs (the Kaplan – Meier method). Based on the results of immunohistochemical staining, the expression of lamin A/C was classified as the negative expression (n = 56) and the positive (n = 70). Log-rank test shows that GC patients with the negative lamin A/C expression

showed significantly poorer prognosis than those with the positive expression. Discussion A-type lamins are essential components of the nuclear lamina [8]. Aside from their structural role in the formation of the nuclear lamina, IMP dehydrogenase lamins A and C are found in the nucleoplasm adjacent to sites of DNA synthesis and RNA processing, suggesting that these proteins could influence both DNA replication and gene expression [2–4]. The A-type lamins, lamins A and C, are synthesized from alternatively spliced transcripts of lamin A gene (LMNA) [9, 10]. A-type lamins are absent in early embryonic development and in certain stem cell populations in adults [11–13] and are expressed only after commitment of cells to a particular differentiation pathway [12, 14]. Mutations in LMNA produce an intriguingly diverse spectrum of diseases including muscular dystrophies (Emery-Dreifuss muscular dystrophy, limb-girdle muscular dystrophy type 1B), neuropathy (Charcot-Marie-Tooth disease type 2), dilated cardiomyopathy with conduction system disease, familial partial lipodystrophy (s.c. fat loss and diabetes), mandibuloacral dysplasia (skeletal malformations and lipodystrophy), atypical Werner’s syndrome, and Hutchinson-Gilford progeria syndrome(precocious aging syndromes) [15–19]. To date, some 200 mutations have been identified in LMNA.

Every descriptor in the regression equation must be independent. The correlation

between each descriptor was calculated and is presented in form of a https://www.selleckchem.com/screening/pi3k-signaling-inhibitor-library.html Pearson correlation matrix in Table 2. As can be seen from these numbers all predictors have a pair correlation minimal covariance <0.5 which assures that any collinearity of predictors is not present. Table 1 reports the AA activity predicted by Eq. 1. A plot of the predicted activity versus the residual values was prepared to determine the existence of systematic errors in the model development (see Fig. B in the Supplementary file). The uniform distribution of residues indicates no systematic error (Belsley et al., 2005). The plots of observed AA activities versus those predicted 4EGI-1 by Eq. 1 together Selleckchem Dinaciclib with the corresponding predicted intervals are shown in Fig. C in the Supplementary file. Compound number 5 is out of 91% prediction threshold and exhibits high AA activity in contrast to other compounds of similar structure having low hydrophobic factor i.e., compounds 2, 4–6. This incidence may be explained by unique structural features. This plot proves that the model as a good descriptive power. Summing up the linear model seems to be adequately fit to the data, all predictors have P < 0.01 and one can conclude that all are independently associated with AA activity. Table 2 Pearson correlation matrix of the parameters used in this study

  JGI4 PCR Hy JGI4 1.00     PCR 0.47 1.00   Hy 0.39 −0.22 1.00 JGI4 Mean topological charge index of order 4, PCR ratio of multiple path count over path count, Hy hydrophilic factor In an attempt to determine the utility of Eq. 1 as model of AA activity four validation analyses were carried out i.e., LOO, LMO, Y-scrambling, and external predictivity (Kiralj and Ferreira, 2009). In the field of statistical techniques the LOO and LMO are used for internal validation. From a theoretically 4��8C acceptable model the R 2 cannot have smaller values than

Q LOO 2 and Q LMO 2 or Q EXT 2 . Overall, the best model is achieved when Q LOO 2  ≤ R 2 ≥ Q LMO 2 and Q LOO 2  ≈ Q LMO 2 . Commonly, Q LOO 2  > 0.5 is considered as proof of the reasonably predictive capability of the equation. Q LOO 2  > 0.7 indicates the stable and predictive potential of the equation. Nevertheless a high Q LOO 2 value does not indicate a high predictive power of the model. On the other hand if R 2 < Q LOO 2 the model is overfitted. As can be seen from the statistics presented next to Eq. 1 in our case R 2 > Q LOO 2 , which means that our model is not overfitted. The LMO test is usually used to verify results obtained from the LOO test. In the Q LMO 2 procedure ten iterations were performed with five molecules left out in each iteration (e.g., tenfold, 80/20 cross validation) (Kiralj and Ferreira, 2009; Tropsha, 2010). The results of the LMO test are collected in Table 3.

The appendix was ligated by means of a transfixive stitch at the base with a 2/0 absorbable suture and the specimen was then cut and extracted by using the finger of a powder-free surgical glove in order to prevent any contamination of the peritoneal PARP signaling cavity or the surgical wound by the infected specimen. Finally, a purse-string suture was placed on the caecum to invaginate the appendicular stump and the cavity was then gently irrigated with at least 2 liters of warm (38°C) normal saline solution and aspirated, focusing on the right iliac fossa, Douglas pouch, the right flank and perihepatic

Q-VD-Oph supplier space. In case of widespread inflammation, a penrose drain was placed on the right iliac fossa according to the surgeon’s criterion. Trocars were then removed, the umbilical hole was closed by means of a 1 Ti-Cron® suture (Covidien Wound Closure) and the skin was sutured with surgical staples. OA requires the same preparation and prophylaxis. The incision may vary depending on the surgeon’s criteria and the characteristics of the patient (Mc Burney, Rockey-Davis or right para-rectal incision). Mesoappendix was ligated by means of a 2/0 silk and a purse-string suture of the same material was placed on the caecum to invaginate the appendicular stump. Lavage with warm saline solution and surgical sponges was performed as deep as the incision would allow. Lavage of the wound

with saline solution was carried out followed by skin closure by means of surgical staples. All data regarding length of hospital stay, morbidity, need for re-consultation in the emergency department after DMXAA order hospital discharge and hospital re-admission were recorded. Patients were classified into four groups according to the type of AA: catarrhalis-phlegmonous appendicitis(FA), gangrenous appendicitis(GA), appendicular plastron with or without localized abscess why (PA) and diffuse appendicular peritonitis (DP). Each group was divided into LA and OA subgroups. Surgical wound infection was defined when a positive culture or purulent discharge was detected or when the wound presented pain or tenderness, localized swelling, redness, or heat, and the incision was deliberately

probed by the surgeon resulting in a positive wound culture. Surgical time was measured from the moment of the skin incision until the closure of the skin. The costs were calculated based on disposable material (Table 1) and hospital stay costs were calculated by means of the center’s clinical information program (“Discharges”), which calculates the cost for the length of stay (LOS), in accordance with the tax regulations of the Valencian regional government, regarding fees for public services based on the DRG and LOS [16]. Table 1 Cost of the material used in OA and LA OPEN APPENDECTOMY Nr. UNITS TOTAL 2/0 silk suture 3 0.4 € 2/0 braided absorbable suture 2 4.3 € Suction device 1 2.3 € TOTAL   7 € LAPAROSCOPIC APPENDECTOMY     Hasson Trocar 1 37 € 5 mm Trocar 2 70 € Endoclinch 1 75 € Lap.

Together, iTRAQ analysis suggests that MucE signaling affected both AlgU-dependent and AlgU-independent protein expression. Conclusions The alternative sigma factor AlgU was responsible for mucE transcription. Together, our results suggest there is a positive feedback regulation of MucE by AlgU in P. aeruginosa, and the expression of mucE can be induced by exposure to certain cell wall stress agents, suggesting that mucE may be part of the signal transduction that MX69 in vitro senses the cell wall stress to P. aeruginosa. Acknowledgements This work was supported by the National Aeronautics and Space Administration West Virginia Space Grant Consortium (NASA WVSGC)

and the Cystic Fibrosis Foundation (CFF-YU11G0). F.H.D. was supported by grants from the NASA Graduate Student Researchers Program (NNX06AH20H), NASA West Virginia Space Grant Consortium, and a post-doctoral fellowship from the Cystic Fibrosis

Foundation check details (DAMRON10F0). T.R.W. was supported through the NASA WVSGC Graduate Research Fellowship. H.D.Y. was supported by NIH P20RR016477 and P20GM103434 to the West Virginia IDeA Network for Biomedical Research Excellence. Electronic supplementary material Additional file 1: Supplementary materials and methods. (DOC 782 KB) References 1. Govan JR, Deretic V: Microbial pathogenesis in cystic fibrosis: mucoid Pseudomonas aeruginosa and Burkholderia cepacia . Microbiol Rev 1996,60(3):539–574.PubMed 2. May TB, Shinabarger D, Maharaj R, Kato J, Chu L, DeVault JD, Roychoudhury S, Zielinski NA, Berry A, Rothmel RK, et al.: Alginate HDAC activation synthesis by Pseudomonas aeruginosa : a key pathogenic factor in chronic pulmonary infections of cystic fibrosis patients. Clin Microbiol

Rev 1991,4(2):191–206.PubMed 3. Leid JG, Willson CJ, Shirtliff ME, Hassett DJ, Parsek MR, Jeffers AK: The exopolysaccharide alginate protects Pseudomonas aeruginosa biofilm bacteria from IFN-gamma-mediated macrophage Baricitinib killing. J Immunol 2005,175(11):7512–7518.PubMed 4. Pier GB, Coleman F, Grout M, Franklin M, Ohman DE: Role of alginate O acetylation in resistance of mucoid Pseudomonas aeruginosa to opsonic phagocytosis. Infect Immun 2001,69(3):1895–1901.PubMedCrossRef 5. Martin DW, Holloway BW, Deretic V: Characterization of a locus determining the mucoid status of Pseudomonas aeruginosa : AlgU shows sequence similarities with a Bacillus sigma factor. J Bacteriol 1993,175(4):1153–1164.PubMed 6. Hershberger CD, Ye RW, Parsek MR, Xie ZD, Chakrabarty AM: The algT ( algU ) gene of Pseudomonas aeruginosa , a key regulator involved in alginate biosynthesis, encodes an alternative sigma factor (sigma E). Proc Natl Acad Sci U S A 1995,92(17):7941–7945.PubMedCrossRef 7. Xie ZD, Hershberger CD, Shankar S, Ye RW, Chakrabarty AM: Sigma factor-anti-sigma factor interaction in alginate synthesis: inhibition of AlgT by MucA. J Bacteriol 1996,178(16):4990–4996.PubMed 8. Damron FH, Goldberg JB: Proteolytic regulation of alginate overproduction in Pseudomonas aeruginosa .

Moreover,

the length of the unmachined region (L U) is equal to 0. Thus, the critical value of V stage is calculated to be half of V tip. Figure 2c,d shows the scratched states after two tip scanning cycles with the conditions of V stage < 0.5V tip and V stage > 0.5V tip, respectively, which will be described in detail as follows: (2) As shown in Figure 2c, when V stage is less than half of V tip, the two regions machined in the adjacent AFM scanning cycles have an overlapping machined region with a length (L O) expressed by Equation 3. If the V stage is small to a certain value, the two adjacent overlapping machined regions also can overlap with each other. As shown in Equation 4, the ratio of L O and L stage can be expressed as an integer (N) plus a fraction (a). BVD-523 concentration From the geometrical relationship, the lengths of the N + 1 and N + 2 times the overlapping machined region can be obtained by 3-deazaneplanocin A cost Equations 5 and 6, respectively. Through Equations 5 and 6, the period of the ladder Selleck Bafilomycin A1 nanostructure is calculated to be L stage. Figure 2e shows the schematic of the cross section of the machined groove with the typical condition of N = 0. L 1 and L 2 represent the lengths of the one and two times machined regions, respectively. h 1 and h 2 are the corresponding depths.

(3) (4) (5) (6) As shown in Figure 2d, when V stage is larger than half of V tip, the two regions machined in the adjacent AFM scanning cycles are nonoverlapping, which can cause a length of the unmachined region (L U) expressed by Equation 7. Through Equations 2 and 7, the period of the ladder nanostructure is also calculated to be L stage. Figure 2f shows the schematic of

the cross section of the machined groove in this condition. h 1 represents one-time machined depth. (7) The real pitch in scratching (Δ) in these two conditions mentioned above can be obtained by Equation 8: (8)   (2) When V stage > V tip, as shown in Figure 3, the scratched state is different from the condition shown in Figure 2. Figure 3a,b shows the machined states of after one and two tip scanning cycles, respectively. Phosphoprotein phosphatase By considering the geometric relationship, as shown in Figure 3b, L C, L U, and Δ can be obtained by Equations 9, 10, and 11, respectively. The length of the unmachined region (L U) only depends on the displacement of the AFM tip in one scanning cycle. From Equations 9 and 10, the period of the ladder nanostructure is calculated to be L stage. Figure 3c shows the schematic of the cross section of the machined groove in this condition. h 1 represents the one-time machined depth. (9) (10) (11)   Matching relations between V tip and V stage under the condition of the stage motion and the feed rate in the opposite direction In this condition as shown in Figures 4 and 5, the feeding direction is along the positive direction of x axis, and the moving direction of the high-precision stage is along the negative direction of x axis.

SD       Cellular Processes: Transport and motor proteins                 6818 Putative coatomer subunit alpha 144 111 813 345 1195 155 5.64 8.30 8703 Myosin-associated selleck chemical protein 152 151 995 598 735 255 6.56 4.84 8711   623 441 3145 2255 2459 906 5.05 3.95 5719 Golgi transport protein 7637 435 2446 1101 7415 learn more 1660 -3.12 -1.03 5728   4330 676 1390 618 3494 1095 -3.12 -1.24 6703   9226 2086 4269 306 7877 3334 -2.16 -1.17 2712 SS1G_01912 13322 4086 3886 2574 5444 711 -3.43 -2.45 7403 KIP1 kinesin-related protein 1494 866 5246 2780 3349 528 3.51 2.24 7804

Vacuolar-sorting-associated protein 25 3952 977 11351 6299 3428 1137 3.57 5.03   Environmental Information Processing: Signal Transduction                 3814 Serine/threonine-prot.

Apoptosis inhibitor phosphatase PP1-1 472 451 270 108 2273 1825 -1.75 4.81 3815   14950 1985 7701 6806 10797 2018 -5.54 1.66 3816   208 94 133 103 745 415 -1.57 3.57 5724 Nucleotide phosphodiesterase 356 91 966 339 607 196 2.72 1.71 0126 14-3-3. DNA damage checkpoint protein 636 515 98 102 2338 2264 -6.49 3.68 0127   261 327 236 252 3161 937 -1.11 12.09 0128   85 79 253 101 904 339 2.98 10.64   Genetic Information Processing                 9206 Ribosomal_L15 19280 5898 6131 5697 9959 8398 -3.14 -1.94 7815 Mediator of RNA polymerase II 1436 1029 2487 788 3794 542 1.73 2.64 6707 Hypothetical protein. DNA helicase 1663 234 785 319 2342 1310 -2.12 1.25 6610 Replication factor C subunit 3 1663 234 785 319 2342 1310 -2.12 1.41 3228 G4P04 (Fragment) 12049 2891 7896 4292 2188 1579 -1.53 -5.51 4803 Calpain-like protease palB/RIM13 1155 494 1308 890 347 171 1.13 -3.33     2072 391 2087 1350 1715 101 1.01 -1.21 7528 Serine/threonine protein kinase (Kin28) 1366 369 2405 840 3280 802 1.76 2.40 7515 Histone acetyltransferase, predicted 3162 819 10965 2273 9410 1514 3.47 2.98 7711 Cell division control protein 25, putative 957 73 2201 1398 2842 659 2.30 2.97   Metabolism                 7407 UDP-xylose

synthase 5850 468 6499 2421 12649 295 1.11 2.16 8507 ATP synthase subunit alpha 13682 2423 11233 8105 4099 3058 -1.22 -3.34 7801 Heat shock protein, putative 1059 268 4202 2317 2373 708 Thalidomide 3.97 2.24   Lipid and Carbohydrate Metabolism                 2523 Acetyl-CoA carboxylase 10538 888 5524 2209 10218 5489 -1.91 -1.03 2524   26474 7704 15933 13733 17308 4885 -1.66 -1.53 3516   38053 5148 12837 8209 26762 5654 -2.96 -1.42 7519 Phosphoglucomutase-1 1967 565 6358 1401 2562 632 3.23 1.30 2319 Acetyl-CoA synthetase 14327 8064 11303 10213 4218 576 -1.27 -3.40 4104 ATP-citrate synthase 18720 2582 14847 10388 11099 2402 -1.26 -1.69 4413 ATP-citrate lyase 9657 987 6925 7702 8736 2536 -1.39 -1.11 6604 Fatty acid synthase 1291 149 285 315 1978 483 -4.52 1.53   Secondary Metabolite/ Carotenoid Biosynthesis                 4515 Phytoene/squalene synthetase 5412 2656 13551 3057 7789 1051 2.50 1.

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