Both methods yielded similar results with estimated copy number of 154–170 copies/cell and of 56–60 copies/cell for pMyBK1 and pMG2B-1, respectively (Figure 5B). Such a difference strongly suggests that the two plasmids have distinct replication and /or regulation systems. Together the 2 M. yeatsii plasmids represent a total extrachromosomal DNA amount of 636 kbp per cell, which is approximately 37% of the total cell DNA. Next, the genetic structure of pMyBK1 was analyzed. The 2 CDSs found in the pMyBK1 sequence (CDSA and B, encoding polypeptides of respectively 519 and 272 aa) showed no homolog

with other mycoplasma plasmids (Figure 2A). The presence of a 192-bp intergenic region buy YM155 between the CDSs as well as the predicted rho-independent

transcription terminator immediately downstream of each CDS strongly suggests that the 2 CDSs are transcribed independently rather than as a single operon. The deduced amino acid sequence of pMyBK1 CDSA exhibits low but significant similarity with mobilization proteins of various bacteria. The N-terminal part of the CDSA protein contains a Mob/Pre domain (pfam01076) typical for relaxases of the MobV superfamily that includes proteins involved in conjugative mobilization and plasmid intramolecular recombination [49]. Sequence alignments with representatives of the MobV family clearly showed that the CDSA protein did possess the three conserved motifs of the family [50] (data not shown). Subsequent phylogenetic analyses

of the CDSA polypeptide with the complete set of MobV proteins described see more by Garcillan-Barcia [51] classified the pMyBK1 protein Florfenicol mTOR inhibitor within the MobV4 relaxase family (data not shown). In contrast to CDSA, no functional domain or characteristic secondary structure was identified in the CDSB-encoded protein. Blast searches revealed that the CDSB protein of pMyBK1 shared significant homology with five chromosome-encoded proteins of Mcc, strain California Kid, or M. leachii, strain PG50 and 99/014/6 but with no known associated function. Identification of the replication protein and the mode of replication of pMyBK1 Since none of the pMyBK1-encoded proteins share homology to known replication proteins, CDSA and CDSB were both regarded as putative candidates. To identify the replication protein and delineate the replication region of pMyBK1, a series of deletion and frameshift mutations were introduced in a shuttle plasmid (E. coli/M. yeatsii), named pCM-H, that was constructed by combining pMyBK1 to a colE1 replicon carrying the tetM tetracycline resistance gene as the selection marker (Figure 2A). The mutated plasmids were then introduced into a plasmid-free M. yeatsii strain (#13156 from the Anses collection) by PEG-transformation, and their replication capacity was measured by the number of resulting tetracycline resistant colonies.

Selective AhR receptor modulator 3,3′-Diindolylmethane (DIM) is a class of relatively non-toxic indole derivatives. DIM is an acid-catalyed consendation product of indole-3-carbinol, a consititudent of cruciferous vegetables, and is formed in the stomach [12]. DIM is an anti-cancer agent, it suppresses cancer cell proliferation in mammary [13], colon [14] and pancreatic [15] cancers. There had been little reports about the effects of DIM on gastric cancer cells growth, the present study was designed to observe

the effects of DIM on gastric cancer cells growth and explore the possible mechanisms. Methods Cell line Human gastric cancer cell line SGC7901 was obtained from the A-1210477 ic50 Cancer Institute of Chinese Academy buy XAV-939 of Medical Science. SGC7901 Cells were maintained in RPMI-1640 medium (GIBCO, Carlsbad, Calif, USA) supplemented with 10% fetal bovine serum (Hyclone, USA), 1 × 105 U/L of penicillin, and 0.1 g/L of gentamycin. The cellular environment was maintained at 50 mL/L CO2 and 37°C. Treatment of cells DIM was purchased from Enzo Life Science company (Bulter Pike plymouth meeting, PA, USA), resveratrol and dimethyl sulfoxide (DMSO) were purchased from Sigma Chemical Company (Bellefonte, PA, USA). DIM and resveratrol were dissolved in DMSO. After incubating for 24 h, one group of cells was treated with DIM at different

concentrations (0, 10, 20, 30, 40, 50 μmol/L) for 24 hours. A second group was treated with DIM (30 μmol/L) plus resveratrol (0, 1, 5, 10, 20 μmol/L) for

6 h. Another group was treated with DIM (30 μmol/L) for different time intervals (0, 1, 6, 24, 48, 72 h), respectively. Control cells received 1 mL/L DMSO only. Reverse transcription–polymerase chain reaction (RT-PCR) After harvesting the cell, total RNA was extracted using the Qiagen RNeasy Mini Kit (Qiagen, Germany) according to the manufacturer’s selleck inhibitor instructions. cDNA was synthesized with 1 μg total RNA using reverse transcriptase, tuclazepam ReverTraAceTM (Toyobo Co., Osaka, Japan) under the following conditions: 30°C for 10 min, 42°C for 20 min, 99°C for 5 min, and 4°C for 5 min. Polymerase chain reaction (PCR) was performed using 2 μl of complementary DNA and 0.6 U Ex Taq DNA polymerase (Takara, Dalian, China ) in 20 μl reaction system and for 30 cycle with 94°C denaturation for 30 s, 55°C annealing for 30 s and 72°C elongation for 45 s. The primer sequences were as follows: reverse transcription–polymerase chain reaction (RT–PCR): AhR, 5’- ACT CCA CTT CAG CCA CCA TC -3’ (forward) and 5’- ATG GGA CTC GGC ACA ATA AA -3’ (reverse), the proposed size of PCR product was 204 bp. CYP1A1, 5’- CCA TGT CGG CCA CGG AGT T -3’(forward) and 5’- ACA GTG CCA GGT GCG GGT T -3’ (reverse), the proposedsize of PCR product was 174 bp.

Quantitative determination of AEG-1 transcript concentrations was performed by real-time RT-PCR with GAPDH as an internal control. Primers for AEG-1 (sense 5′ GGC AAT TGG GTA

GAC GAA GA 3′; antisense 5′ CCT GTT TTG GAC GGG TTT TA 3′) and GAPDH (sense 5′ GAG TCA ACG GAT TTG GTC GT 3′; antisense 5′ TTG ATT TTG GAG GGA TCT CG 3′) synthesized by Sangon (Shanghai, China) and were used to measure gene expression. Amplification reaction assays were set up triplicate for each sample using the SYBR Green system (TaKaRa, Dalian, China). In order to quantify the gene expression changes, the ΔΔCt method was used Selleck BAY 80-6946 to calculate the relative fold-changes normalized against GAPDH. Western blot analysis After 48 hours of transfection, cells and supernatant of each group would be collected. Proteins were extracted after break-down

of cells by SDS boiling method. Proteins were quantified by Bradford method. 50 μg of protein underwent GF120918 concentration SDS-PAGE and was transferred to PVDF membrane BIBF 1120 cell line afterward. It was then sealed at room temperature for 2 hours. The primary antibodies, rabbit anti-human AEG-1 antibody (Invitrogen, Carlsbad, CA), was added at a ratio of 1:1000, and incubated overnight at 4°C. The membrane was washed with PBS. Then, the secondary antibody, mouse anti-rabbit IgG/HRP antibodies (Amersham Biosciences), was added at a ratio of 1:5000, and incubated at room temperature for 2 hours. The membrane was washed three times and reacted with chemiluminescent agent for 5 minutes. tetracosactide It was then ECL tabletting, exposed, and displayed. The amount of each protein sample was controlled by β-actin. Cell proliferation assay M17 and SK-N-SH cells were transfected in 6-well plate. 24 hours late, the transfected cells were trypsinized and plated

in 96-well plates with 1.0 × 103 cells in 100 μl of the medium and allowed to attach for 24 h, then 10 μl of MTT (5 mg/ml in PBS) was added for 4 h incubation at 37°C after 4, 24, 48, 72 h, respectively. Subsequently the formazan crystals were solubilized with 100 μl of 10% sodium dodecyl sulfate (SDS) in 0.01 M HCl for 24 h. The absorbance was measured using a Microplate Reader (Bio-rad 680, Bio-rad, USA) with a test wavelength of 570 nm and a reference wavelength of 630 nm and all experiments were performed in triplicate. The cell proliferation curve was plotted using the absorbance at each time point. Colonogenic assay The number of colonies was determined as described previously [12]. Briefly, following transfection for 48 h, cells were trypsinized, counted, and seeded for the colony forming assay in 60 mm dishes at 200 cells per dish. After incubation for 14 days, colonies were stained with crystal violet and the numbers of positive cells counted. Colonies containing more than 50 cells were scored, and triplicates containing 10–150 colonies/dish were counted in each treatment.

The grade determined by the remote physician was not communicated to the on-site physician, who was then asked to grade all the injuries at the end of the operative procedure. The two grades were compared to determine the accuracy of the remote physician in grading traumatic injuries through the telepresence robot. Descriptive statistics Selleckchem VS-4718 was used to analyze all survey results. Institutional CP673451 research buy Review Board The study was reviewed and approved by the University of Miami Institutional Review Board, the Jackson Memorial Hospital Clinical Research Review Committee and the Department of Defense

Human Research Protection Office. Results Data was collected on 50 surgical cases, both emergency (80%) and elective cases (20%). Patients were classified as trauma (70%) and non-trauma patients (30%). The majority of cases (64%) were emergency surgery on trauma patients, almost evenly distributed between penetrating (49%) and blunt trauma (51%). 40% of non-trauma cases were hernia-related Participants included 13 attending physicians and 9 fellows. There was a varied distribution of injuries and operative anatomical structures (Table 1) Table 1 Injury location distribution   # of cases   # of cases Trauma selleck inhibitor Patients Non-Trauma Patients Head 1     Neck   Abdomen   Larynx 1 Wall 2     Inguinal Hernia

5 Chest   Ventral Hernia 2 Wall 4 Small bowel 3 Rib Selleckchem Atezolizumab 1 Spleen 1 Vena Cava 1     Subclavian Artery/Vein 2 Inguinal Lymph Node 1 Abdomen   Unspecified 1 Wall 3     Stomach 1     Spleen 4     Bladder 1     Kidney 1     Small Bowel 4     Colon 5     Unspecified 2     Extremities 3     Miscellaneous       Skin graft

1     Remote physicians reported a high level of satisfaction with the use of the telepresence robot (Figure 3). Almost all remote participants (94%) agreed or strongly agreed being able to see the procedure well (Figure 4). The only times the remote clinician noted having difficulties visualizing the procedure occurred when the operating table was surrounded by a team of clinicians. Internet connectivity was an issue in 24% of the cases, ranging from minimal interruption to slow connection speeds. Crowding in the operating room obstructed the view for the remote physician in less than 20% of the cases; however, due to the slim design of the robot it could be moved to either the foot or head of the bed without interference. 94% of remote physicians and 74% of local physicians felt comfortable communicating via the telepresence system (Figures 5 and 6). To measure the value of the telepresence robot, we compared its use to that of the telephone. The most significant finding from the study is that all the local clinicians agreed that having access to a remote expert would be beneficial, and that to do so it would be more effective through telemedicine rather than just the telephone (Figures 7 and 8).

Panels varied in their

individual constituents, and in the number of components. Generally the values of AUROCs of panel tests in patients with ALD in predicting cirrhosis /sever fibrosis are comparable with those in NAFLD or Hepatitis C. For example in a metaanalysis of Fibrotest in Hepatitis C the mean AUROC for predicting significant fibrosis was reported as 0.77 (95% CI 0.75, 0.79) and in NAFLD 0.81 (95% CI 0.74 0.86) [2], and a summary AUROC for cirrhosis 0.82 [32]. phosphatase inhibitor library Certain panels such as APRI seem to perform less well in ALD than in Hepatitis C. Summary AUROC for significant fibrosis was reported as 0.76 (95% Veliparib CI 0.74 0.79) and for cirrhosis 0.82 (95% CI 0.79 0.86) [33, 34]. There have been reports in the literature of the effect of current heavy alcohol consumption on circulating serum markers which may limit their performance in identifying the chronic effect of alcohol on fibrosis in patients who may be current drinkers. The mode of action of alcohol on the markers is unclear. Animal models have shown that alcohol may have an effect on serum markers such as HA in several ways- by alteration of communication between liver cells thereby affecting HA clearance and by direct effect on induction of hepatic sinusoidal endothelial cell dysfunction [35, 36], Studies

have shown that some markers are more susceptible to influences of acute consumption but results FRAX597 are not consistent. One study reported that some markers are affected (tenascin, laminin), some are unaffected (PIIINP, TIMP1), and some very variable (HA) [37]. One small study reported that mean levels of PIIINP but not TIMP1 rise with abstinence [38]. This confirmed the results from an earlier study which showed similar effect of alcohol on PIIINP [38] Direct studies of effects of alcohol on

serum markers in clinical studies involve very small numbers and few studies have reported in the last 5 years. Most alcohol status (were reported ) is self report with some studies using collateral evidence when available. The included studies in this review did not all report current drinking status in detail. Tyrosine-protein kinase BLK In 4 studies included patients were in-patients for alcohol withdrawal /rehabilitation, in 2 studies the patients were not abstinent. More data from large robust studies are needed to properly evaluate the influence of current alcohol intake (ideally quantified with objective measures/triangulated evidence) on markers, reporting results in terms of level of alcohol consumption and time of abstinence. A major concern in drawing overall conclusions from this review is the considerable heterogeneity of the study populations. Whilst all included studies recruited patients from specialist clinics in secondary or tertiary settings (there were no studies set in primary care), there was variation in the population characteristics, such as level of alcohol consumption, and differences in the prevalence of severe fibrosis.

The consensus of LxxLxCxxNxLxxLDLxxNxx in which “”L”" at position 16 is more frequently occupied by Val or Ile than by Leu is observed in some proteins. They include Listeria lmo0331 homologs, CHU_0515 from Cytophaga find protocol hutchinsonii and PORUE0001_1723 from Porphyromonas uenonis 60-3 (Figure 1G). Also, the GANT61 mouse pattern of LxxLxCxxNxLxxLDLxxLxx is observed in TDE_0593, TDE_2231, and TDE_2003 from Treponema denticola (Figure 1H, and Additional file 2, Figure S1). Moreover, the pattern of LxxLxCxxNxLxxLDLxxVxx is observed in Pnap_3264 from Polaromonas naphthalenivorans

and MldDRAFT_4836 from Delta proteobacterium MLMS-1 (Figures 1I and 1J, and Additional file 2, Figure S1). The coexistence of the first and the second subtypes is observed in the LRR domains in at least six IRREKO@LRR proteins. They include KAOT1_04155 from Kordia algicida OT-1, COPEUT_03021 from Coprococcus eutactus ATCC 27759, Fjoh_1188/FjohDRAFT_4748 and Fjoh_1189/FjohDRAFT_4747 from Flavobacterium johnsoniae, RUMGNA_03120 from Ruminococcus gnavus ATCC 29149, DORFOR_03338 from Dorea formicigenerans ATCC 27755, and internain-J homologs from eleven Listeria monocytogenes strains (Figures 1K and 1L, and Additional file 2, Figure S1). Nested periodicity of IRREKO@LRRs IRREKO@LRRs show a characteristic, nested periodicity; the domains consist of alternating 10- and 11- residue units of LxxLxLxxNx(x/-).

To confirm this periodic nesting we performed detailed sequence analysis of IRREKO@LRR selleck compound proteins using dot plots analysis and a radar chart analysis. Self dot plots were performed for four IRRECO@LRR proteins – BIFLAC_05879 from Bifidobacterium animalis, A1Q_3393 from Vibrio harveyi HY01, lmo0331 protein from Listeria monocytogenes and an internalin-related protein, TDE_0593, from Treponema denticola – (Additional file 3, Figure S2). The self dot plots indicate that these proteins demonstrate tandem repeats of short residues that is ~10-11 residues long,

in addition to tandem repeats of IRRECO@LRR with 21 residues. Radar charts were drawn for three families of IRREKO@LRRs proteins, in which second the occurrence frequency of amino acids is compared between positions 1-10 and positions 11-21. Figure 2A shows a radar chart of Vibrio proteins. Seven Vibrio species encode twelve IRREKO@LRR proteins which are potential homologs (Additional file 1, Table 1). The IRREKO@LRRs domains in their proteins contain 158 LRR repeats. One hundred thirty-seven of the 158 repeats are complete “”IRREKO”" domains with 21 residues. The radar chart of the 137 LRRs is shown in Figure 2. As expected, “”L”" at positions 1, 4, and 6 is highly conserved with positions 11, 14 and 16, respectively. In addition, a significant, weak conservation is observed between positions 10 and 21 but not 20, because amino acid distribution of positions 10 and 21 is very similar and are relatively rich in Lys, Asn and Gln.

J Am Geriatr Soc 47:850–853PubMed 42. Cumming RG, Ivers R, Clemson L, Cullen J, Hayes MF, Tanzer M, Mitchell P (2007) Improving vision to prevent falls in frail older people: a randomized trial. J Am Geriatr Soc 55:175–181CrossRefPubMed 43. Society AG, Society BG, AAoOSPoF P (2001) Guideline for the Prevention of Falls in Older People. Journal of the American Geriatrics Society 49:664–672CrossRef 44. Gates S, Fisher JD, Cooke MW, Carter YH, Lamb SE (2008) Multifactorial assessment and targeted intervention for preventing falls and injuries among older people in community and emergency care settings: systematic review and meta-analysis. BMJ

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Med 70:417–421CrossRefPubMed”
“Introduction Natural products 3-MA cell line derived from plants have received extensive attention as potential anti-cancer agents over few decades. Most of current anti-cancer drugs such as camptothecin, vincristine, taxol, etoposide and paclitaxel are plant-derived compounds [1, 2]. These bioactive phytochemicals are known to exert find more their anti-cancer activity through different mechanisms, including AZD5582 manufacturer altered carcinogen metabolism, induction of DNA repair systems, immune activation, suppression of cell cycle progression and induction of apoptosis. Several studies have shown that natural products rich in polyphenols have strong chemopreventive and chemotherapeutic properties in different types of cancer cells [3, 4]. Flavonoids, polyphenolic compounds found in plant-derived dietary components, exhibit multiple biological activities, including anticarcinogenic activity. Luteolin, one of the most effective flavonoids, can delay or block the development of cancer cells in vitro and in vivo via inhibition of tumor cell proliferation, induction of cell cycle arrest and apoptosis by inhibiting enzymes involved in cell activation such as phosphodiesterases kinases and DNA topoisomerases [5]. Methylation

Glycogen branching enzyme of CpG islands is an important component of the epigenetic code and a number of genes become abnormally methylated during tumorigenesis. A hypermethylation of the tumor suppressor gene p16 INK4A at its CpG-rich promoter regions and subsequent inactivation of the p16 INK4A gene have been reported in several haematological and solid cancers [6, 7]. This hypermethylation targets the expression of specific genes involved in the DNA damage response including, the retinoblastoma protein (pRB) [8]. More recently, many studies have reported that UHRF1 serves as a fidelity factor for the maintenance of the DNA methylation pattern throughout cell duplication [9, 10]. The Set and Ring Associated domain (SRA domain) of UHRF1 has the unique feature to recognize a particular state of DNA, i.e.

% from Cu(NO3)2) showed a minimum lattice strain (Figure 2b). This result suggests that the Cu dopants in sample S4 took proper sites in the ZnO lattice. Generally, the substitution of Zn2+ by Cu2+ would lead to a change in the lattice parameters [18, 27]. However, the pronounced changes in the lattice strain when Cu(NO3)2 is used as the Cu precursor (samples S4 and S5) suggest that the concentration of OH− in the aqueous solution plays an important role in the crystalline quality of the grown nanorods. Figure 2

Crystallite size (a) and lattice strain (b) of undoped and Cu-doped ZnO nanorods. Morphology The morphology of the nanorods was investigated NSC23766 concentration by scanning electron microscopy. The top-view SEM images for the undoped and Cu-doped

ZnO nanorods are shown in Figure 3. The density and diameters of the nanorods showed dependency on Cu precursor and concentration. It can be seen that the average rod diameter increases from approximately 75 nm for undoped nanorods (sample S1) to approximately 210 nm when 1 at.% Cu is added from Cu(CH3COO)2 (sample S2),while when 2 at.% (sample S3) is added from the same precursor, the nanorods aggregated and the structure becomes compact. On the other hand, when 1 at.% of Cu (sample S4) is added from Cu(NO3)2, the average nanorod diameter increases slightly relative to the undoped nanorods. Increasing the Cu content to 2 at.% (sample S5) from Cu(NO3)2, the average nanorod diameter increases to approximately 120 nm. Figure 3 SEM images of the undoped and Cu-doped ZnO nanorods. The variations in the nanorod diameters and densities as functions of Cu concentration and precursors selleck are explained in Figure 4a,b. The ZnO unit cell is shown in Figure 4a, where the cations (zinc ions) and the anions (oxygen ions) are arranged alternatively along the c-axis perpendicular to the substrate. Basically,

the nanorod diameter and density are highly affected by the density of the nucleation sites and the pH value of the aqueous solution. Therefore, PKC inhibitor introducing Cu dopants into the reaction path would increase the nucleation density and hence enhance the growth rate, which in turn, results in a coarsening and lateral medroxyprogesterone aggregation of the nanorods. Figure 4 Schematics of ZnO unit cell (a) and nanorod growth and aggregation (b). The reason why the nanorods doped with Cu(CH3COO)2 exhibited a larger diameter compared to the nanorods doped with the same concentration of Cu(NO3)2 is that as shown in Equations 2 and 3, both Cu(CH3COO)2 and Cu(NO3)2 release the same concentration of Cu2+. Therefore, the anion concentration is a determinant factor. (2) (3) The two different anions CH 3 COO − and will affect the nanorod growth process in different ways. In the hydrolysis process of CH 3 COO−, more OH− will be released when the amount of OH− in the aqueous solution decreases (Equation 4). Accordingly, both lateral and vertical growth rates will increase with the increase of Cu(CH3COO)2.

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Amino acid sequencing The N-terminal amino acid sequence of mTOR inhibitor TanLpl, TanLpa, and TanLpe were determined by automated Edman degradation using a PPSQ-10 protein sequencer (Shimadzu, Kyoto, Japan). Effects of pH and temperature on tannase

activity The activity of the purified recombinant TanLpl, TanLpa, and TanLpe on pH and temperature was determined in comparison with that of a commercially available A. oryzae tannase (Wako). All reaction mixtures contained 600 nM of the purified tannase and 1 mM MG as a substrate. The optimal pH of the enzyme was determined at 37°C for 15 min in the range of pH 4.0–10.0 using the following buffers: 50 mM sodium citrate buffer (pH 4.0–5.5), 50 mM phosphate buffer (pH 6.0–7.0), 50 mM Tris–HCl buffer (pH 7.5–8.5), and 50 mM NaHCO3 buffer (pH 9.0–10.0). The optimum temperature was determined by measuring the tannase activity at 20–55°C in 50 mM Tris–HCl (pH 8.0) for TanLpl, TanLpa, and TanLpe, and in 50 mM sodium citrate (pH 5.5) for A. oryzae tannase. The reaction products were analyzed by high performance liquid chromatography (HPLC) as described previously [17]. One unit of tannase Epacadostat mouse activity was defined as the amount of enzyme required to release 1 μmol of gallic acid in 1 min under specified conditions. Effects of various chemicals on tannase activity Effects of various

metal ions (CaCl2, MnCl2, FeSO4, MgSO4, ZnSO4), EDTA, urea, β-mercaptoethanol, and phenylmethylsulfonyl fluoride (PMSF) on the lactobacilli tannase activities were investigated. Activity of each enzyme was estimated using 1 mM MG as substrate with 1 mM each of the above chemicals at 37°C for 15 min under the predetermined optimal pH condition. The reaction products were analyzed by HPLC as described above. Kinetic constant of Lactobacilli

tannase The reaction mixture (200 μl) was prepared in 50 mM Tris–HCl (pH 8.0) for TanLpl, TanLpa, and TanLpe, or 50 mM sodium citrate (pH 5.5) for A. oryzae tannase, containing each of the substrates (0.1–4 mM), and the enzyme (33 Meloxicam nM). The mixture without enzyme was once preincubated at 37°C for 10 min, and the reaction was started by adding the enzyme. After incubation at 37°C for 15 min, the reaction was stopped by adding 20 μl of 20% (v/v) phosphoric acid to be subjected directly to HPLC analysis. K m and V max values were calculated from a Hanes–Woolf plot. k cat value was calculated based on the molecular mass of each tannase enzyme (deduced from the gene sequences and SDS-PAGE). Nucleotide Sequence Accession Number The nucleotide sequences reported in this study has been submitted to DDBJ/EMBL/GenBank under the accession number listed in Additional file 1: Table S1. Results Sequence analysis of tanLpl, tanLpa, and tanLpe The full-length nucleotide sequence of the tanLpa (1410 bp) of L. paraplantarum NSO120 and tanLpe (1413 bp) of L. pentosus 22A-1 as determined by inverse PCR predicted proteins of 469 and 470 amino acid residues, with molecular mass of 50,708 Da and 51,193 Da, respectively.