All predictors except spasticity were treated as continuous

variables in the logistic regression (Royston et al 2009). The predictors were entered in the initial model for multivariate analysis. Initially we used a bootstrap variable selection procedure that retained those variables selected with backwards stepwise regression (p to remove = 0.2) in at least 80% of bootstrap samples. Regression coefficients were zerocorrected to reduce bias ( Austin 2008). However, two of the three bootstrap models obtained in this way had poor calibration (Hosmer-Lemeshow p < 0.05). We therefore used, instead, a conventional backwards stepwise regression variable selection procedure (p to remove = 0.05) to develop our final models. Discrimination (how well the Lapatinib supplier model can identify patients with and without outcomes) was quantified with

area under the receiver-operating curves (AUC). Calibration (how well observed probabilities agree with predicted probabilities) was evaluated by inspecting the slope of the observed-predicted graphs and with the Hosmer-Lemeshow statistic ( Royston et al 2009). All analyses were conducted using Stata 11.1. The flow of participants through the study is shown in Figure 1. Baseline measures were obtained at a median of 6 days (IQR 3 to 11) after stroke. Final outcome Enzalutamide in vivo measures were measured at a median of 6.1 months (IQR 5.9 to 6.4) after stroke. Patients who were able to ambulate independently (n = 59), or move a cup (n = 135), or feed themselves (n = 131) with the hemiplegic arm at

baseline were excluded from subsequent analyses of recovery in these abilities, respectively. Twenty of the remaining participants died, four declined re-assessment, and three could not be contacted (Figure 1). Consequently the overall rate of follow up was 81% for ambulation, 78% for moving a cup, and 81% for feeding. In participants who survived, the rate of follow up was 94% for ambulation, Endonuclease 94% for moving a cup, and 97% for feeding. Characteristics of patients are shown in Table 1. Of the 114 stroke survivors who were unable to ambulate initially, 80 (70%, 95% CI 62 to 79) were able to do so at six months. Of the 51 stroke survivors who were unable to move a cup across the table initially, 21 (41%, 95% CI 27 to 55) were able to do so at six months. Of the 56 stroke survivors who were unable to feed themselves with a spoonful of liquid initially, 25 (45%, 95% CI 31 to 58) were able to do so at six months. Results of univariate analyses are shown in Table 2. Odds ratios are associated with a one-unit increase in the predictor. Both severity of stroke and motor function (standing up ability and combined motor function of arm) were significantly associated with recovery of ambulation and feeding oneself. A one-unit increase in the NIHSS was associated with a 15% reduction in odds of recovering ambulation. A one-unit increase in Item 4 of MAS was associated with a 2.

In the first year of life there was a progressive decline in the titre of acute phase neutralising antibodies, which coincided with an increase in convalescent titres over the same period (Fig. 1a). The incidence of severe RSV associated pneumonia during the study period

rose sharply after birth; starting at 1108 admissions/100,000 child years of observation (cyo) at between 0 and 1.9 months of age (95% CI: 906–1310) and peaking at 1378 admission/100,000 cyo (95% CI: 1140–1616) at between 2 and 3.9 months of age. The incidence of severe RSV pneumonia thereafter declined to 934 admissions/100,000 cyo (95% CI: 740–1128) in the selleck products 4–5.9 month age class, and was lowest in the 6–11.9 and 12–41.9 selleck screening library month age classes at 499 admissions/100,000 cyo (95% CI: 420–578) and 56 admissions/100,000 cyo (95% CI: 46–65), respectively, as shown in Fig. 1b. In the

first year of life the response to infection, measured as fold change in neutralising antibody titre from the acute to convalescent phases of infection, increased progressively with age. In the first 2 months of life (0–1.9 months), there was a significant decline in the neutralising response, i.e., fold change less than unity (p = 0.02; Fig. 1), while no significant change in titre was observed at 2–3.9 months of age (p = 0.1). However, as shown in Fig. 1b, in all age classes of children older than 4 months of age, there was a significant rise in the titre of neutralising antibodies following natural infection. The proportion of infants who had a detectable rise in titre from the acute to convalescent phases of infection (-)-p-Bromotetramisole Oxalate (fold change in titre >1) increased with age as shown in Fig. 2. In the youngest age class (0–1.9

months old), only 26% of infants with a confirmed RSV infection had a rise in titre following infection. In subsequent age classes, the proportion of infants with a detectable rise in the titre of neutralising antibodies following infection rose sharply with age, reaching 66% in the 2–3.9 month age class and 60% in the 4–5.9 month age class. The greatest response was observed in the 6–11.9 month age class where all infants had detectable rises in titre following infection. The same trend was observed when the data were analysed in terms of infants who generated an antibody response that reached or exceeded the 4-fold seroconversion threshold. No seroconversions were observed in the youngest age class (0–1.9 months old). However in subsequent age classes the rate of seroconversion steadily increased with age. Seroconversion rates in the 2–3.9, 4–5.9, 6–11.9 and 12–41.9 months of age were 11%, 33%, 62% and 50% respectively.

, 2012). Thus, there is an imperative need for effective treatments for childhood PTSD. This review highlights one of the few examples where research in animals has helped lead to treatments

for human brain disorders. Since the PFC expands greatly in evolution, work in nonhuman primates has been particularly important for revealing the molecular mechanisms to protect and normalize PFC physiology in humans. Continued research is needed to help develop treatments that alleviate the suffering of patients exposed to trauma. AFTA is supported by an NIH Director’s Pioneer Award DP1AG047744-01. The research described in this review has been funded by a wide variety of sources. Disclosures: AFTA and Yale University receive royalties from Shire Pharmaceuticals from the sales of Intuniv™ (extended release CHIR-99021 ic50 guanfacine) for the treatment of pediatric U0126 manufacturer ADHD. “
“The acute stress response, characterized by activation of the sympathetic nervous system, the hypothalamus-pituitary-adrenal axis and the

immune system, is a physiologically adaptive response that enables the organism to deal with environmental threats. However, when the stress exposure is chronic, prolonged activation of the stress response may become maladaptive and have adverse consequences for the individual. In addition to disorders directly linked to stress exposure, like post traumatic stress disorder, risk of the development of whatever several other disorders such as affective disorders, type 2 diabetes and cardiovascular disease have been associated with stress (reviewed in (de Kloet et al., 2005)). Chronic stress during adulthood may have adverse consequences, but the effects of stress exposure during gestation or early childhood may have more severe consequences as it may alter brain development and thereby have long-term consequences on adult phenotype. The idea that the early life environment may alter adult phenotype is described in the Developmental Origins of Health and Disease (DOHaD) hypothesis. This hypothesis states that adverse conditions during the early life period may result in persistent changes in physiology and metabolism that in

turn alter risk for disease development in adulthood and was first proposed by David Barker (Barker, 1988). Therefore, this hypothesis was initially referred to as the “Barker Hypothesis”. This hypothesis was based on the observation that low birth weight was associated with increased risk for coronary heart disease in adulthood (Barker and Osmond, 1986). Over the last decades more data supporting this hypothesis have become available from studies in both humans as well as in animal models. Evidence that this hypothesis may hold true comes from epidemiological studies in individuals who were exposed to adverse environmental conditions, like natural disasters or war, showing increased risk for metabolic, immune and stress-related disorders later in life.

001), gender (p < 0.001), and logarithm of time between blood collection and MMR (p < 0.001). The rates of seroconversion for measles were 98.2% in the group with simultaneous YFV and MMR, and 99.2% among those who received YFV 30 days or more after MMR (p = 0.090). GMTs were 3.44 IU/mL (95% CI: 3.20–3.70 IU/mL) and 3.19 IU/mL (95% CI: 3.00–3.39 IU/mL), respectively. The seroconversion and GMTs were similar across groups who got

different substrains of YFV: 98.9% seroconversion and GMT of 3.35 IU/mL (95% CI: 3.13–3.58 IU/mL) in children in the 17D-213 group; 98.4% seroconversion and GMT equal to 3.28 IU/mL (95% CI: 3.07–3.51 IU/mL) in the 17-DD group (p = 0.521). The rates of seroconversion for mumps were 61.1% in the group with simultaneous BMS-354825 molecular weight YFV and MMR, and 70.8% among those who received YFV 30 days or more after MMR (p < 0.001). GMTs were 335.5 mIU/mL (95% CI: 314.4–358.0 mIU/mL) and 414.1 mIU/mL (95% CI: 388.0–442.1 mIU/mL), respectively. The seroconversion and GMT were similar across groups who got different substrains of YFV: 67.0% seroconversion and GMT of 384.7 mIU/mL (95% CI: 359.9–411.2 mIU/mL) in children in the 17D-213 group; 65.2% seroconversion and GMT equal to 362.6 mIU/mL (95% CI: 340.0–386.7 mIU/mL)

in the 17-DD group (p = 0.497). Reverse cumulative distribution curves for antibody titers after Torin 1 in vitro MMR, support the finding of similar immunogenicity across groups defined by YFV substrains, and groups in which YFV and

MMR were given either simultaneously or 30 days apart (data not shown). For mumps, the curves were also consistent about with the small difference in the GMT shown above. For each of the three components, the proportions of seroconversion, did not differ substantially in children who received MMR vaccine from different producers, whereas GMTs were slightly higher among those who received the MSD vaccine (data not shown). The proportion of seroconversion and magnitude of immune response (GMT and distribution of postvaccination antibody titers) were greater in the group vaccinated with an interval of 30 days compared to simultaneous vaccination (p < 0.001, Table 3 and Fig. 2). In contrast, the groups defined by the types of yellow fever vaccines showed no significant difference in immune response (p > 0.5, Table 2 and Fig. 2). The logistic model (data not shown) showed a strong association of seroconversion (OR = 4.53, 95% CI: 3.12–6.57) and post-vaccination seropositivity (OR = 7.60, 95% CI: 5.06–11.40) with the interval between administration of YFV and MMR, adjusted for the interval between blood collection and vaccination with MMR. In multivariate linear model (data not shown) log10 post-vaccination antibody titers against yellow fever were strongly correlated to the interval between YFV and MMR (p < 0.001), adjusted for the time interval between blood collection and MMR vaccine (p < 0.001).

Table S2.   CD4+ T-cell response to the F4/AS01 vaccine: Responder rates.a Vaccine-induced CD4+ T-cells exhibited a polyfunctional phenotype (Fig. S2). In ART-experienced subjects, approximately 75% of F4-specific CD40L+CD4+ T-cells secreted ≥2 cytokines and approximately 35% secreted ≥3 cytokines and this cytokine coexpression profile was maintained until month 12. A similar trend was observed in ART-naïve subjects; however, results in this cohort must be interpreted with caution due to the low frequency of F4-specific CD4+ T-cells induced (data not shown). Supplementary Fig. II.   (a) Cytokine co-expression profile of F4-specific CD40L+CD4+ T-cells at pre-vaccination and two weeks post-dose

2 (day 44) in vaccinated ART-experienced

patients Volasertib cell line (black line represents median value), (b) with pie charts for all time-points. Results are expressed as the percentage of F4-specific CD40L+CD4+ T-cells expressing 1, 2 or 3 cytokines (IL-2, TNF-a or IFN-γ). High levels of HIV-1-specific CD8+ T-cells expressing signaling pathway mainly IFN-γ were detected at baseline in both cohorts. Irrespective of the marker tested or the stimulatory peptide pools used, no increase in HIV-1-specific CD8+ T-cell frequency or change in the expression profile of CD8+ T-cell activation markers was detected following vaccination in either cohort (data not shown). Pre-existing IgG antibodies against the F4 fusion protein and against all four of the individual vaccine antigens were detected in both cohorts. Vaccination increased antibody levels against the F4 fusion protein and all individual vaccine antigens in ART-experienced subjects, but not in ART-naïve subjects who had higher pre-vaccination titres compared to ART-experienced subjects (Fig. S3). Supplementary Fig. III.   Humoral response (median geometric mean antibody concentration [GMC] with 95% CI) to vaccination (according to protocol cohort for immunogenicity); (a) overall response to F4 in ART-experienced

and ART-naïve subjects; (b) medroxyprogesterone response to specific antigens in ART-experienced subjects; (c) response to specific antigens in ART-naïve subjects. Absolute CD4+ T-cell counts were variable over time in both cohorts. Ad hoc comparisons of change from baseline detected no significant differences between vaccine and placebo groups at any time-point in either cohort (data not shown). Except for two minor blips in the vaccine group and one minor blip in the placebo group, viral load remained suppressed in both groups of ART-experienced subjects over the 12 months of follow-up. In ART-naïve subjects, ad hoc comparisons of change in viral load from baseline indicated a significant difference in favour of the vaccine group, in which a transient reduction in viral load from baseline was observed two weeks post-dose 2 (p < 0.05) ( Fig. 2). This difference was sustained over the 12 months of follow-up, but was only statistically significant at two weeks post-dose 2.

3 Thus, amplified products of TK and TMP kinase were purified with NP-PCR purification kit, Taurus Scientific, USA and were sequenced by dye terminating method at MWG

Biotech India Ltd and the sequences were deposited at GenBank www.ncbi.nlm.nih.gov. The cloning of TK and TMPK learn more genes were carried out as described earlier.19 The TK and TMPK genes were expressed using 1 mM IPTG from clones HTK and HTM respectively and pure rTK and rTMPK were obtained from respective clones were analyzed and characterized.17, 18 and 19 TK and TMPK annotated protein sequences of S. aureus ATCC 12600 were analyzed by using the Internet available free softwares – NCBI BLAST, Bio-edit, Mega 4.1 and Clustal X. 20, 21 and 22 The translated TK and TMPK protein sequences were submitted to BLAST-P for similarity searching to find out its homologs. 20 Pairwise and multiple sequence alignment were performed using Clustal X. 21 The phylogenetic tree produced by the multiple sequence alignment was analyzed by using MEGA 4.1. 22 The protein sequences were scanned against Pfam database to identify the conserved

domains and family information of the proteins. 23 The TK and TMPK structures of S. aureus were retrieved from (PDB IDs: 3E2I and 4DWJ) and were superimposed with human TK and TMPK (PDB IDs: 1XBT and 2XX3) using MATRAS program. 24 The extent of UMI-77 mouse homology between the structures was represented by respective RMSD values. The TK and TMPK which are prominent enzymes involved in the formation of dTMP and dTDP respectively play critical role in the proliferation and pathogenesis of S. aureus in the human host especially in relapsed episodes and in SCV. 4, 5 and 6 TMPK is an enzyme which

is in junction between de novo biosynthesis and salvage pathway and therefore, obtains substrates from both the pathways. The enzyme kinetics results of TK and TMPK ( Table 2 and Table 3) indicated that these enzymes are actively present in this pathogen ( Supplementary Figs. 1 and 2). The TMPK and TK genes in the clones HTM and HTK respectively were confirmed by PCR using the primers mentioned in Table 1 and the insert in the clones were sequenced (GenBank accession numbers FJ415069 and FJ232923). The pure recombinant proteins eluted from nickel metal chelate agarose column (Bangalore Genei Pvt Ltd) exhibited single band in SDS-PAGE (10%) with a molecular Calpain weights of 21 kDa and 20 kDa respectively17 (Fig. 1). The structural superimposition results of S. aureus TK and TMPK and human TK and TMPK structures 24 indicated RMSD values of 0.913 Å and 1.336 Å respectively showing close homology between the structures ( Fig. 3 and Fig. 5). However, TMPK structure of S. aureus exhibited typical characteristics of a class II enzyme, containing a G at position x1 of the P-loop whereas R is present in human TMPK and a series of basic residues (R 141, R 147, R 151 and K 144) in the LID region of S. aureus TMPK.

The American view [6] is much clearer, specifying relative contra-indications under clinical, social and procedural categories. Clinical contra-indications in the US include thyrotoxicosis and pre-existing vocal paresis alongside criteria applicable to any day case procedure (cardiorespiratory co-morbidity, morbid obesity, etc.). Social factors consider the home Palbociclib price environment, availability of primary carer, distance

from hospital, communication difficulties, patient preference and understanding. Within the procedural category, contra-indications include large volume glands and retrosternal extension, plus specific intra-operative factors to reduce the risk of complications; anaesthetic choice, type and extent of surgery, nerve monitoring, haemostasis, parathyroid gland management, wound closure and extubation. For safe postoperative care, there are suggested discharge criteria (absence of neck swelling, dysphagia etc.) and emphasis on the importance of nursing and patient/carer education for the recognition of complications. Unilateral

surgery compared to total thyroidectomy carries a reduced risk of laryngeal nerve dysfunction, postoperative hypocalcaemia and potentially a reduced risk of bleeding and its consequences given the smaller operative field. Indeed, unilateral surgery has been suggested as generally more suitable [16] and [19]. An Austrian groups’ review of over 30,000 thyroidectomies [24] would appear to support this position since no patient in their review developed Anti-diabetic Compound Library chemical structure a haematoma after undergoing unilateral

surgery (92 of 8783 procedures, 1% cases) or became symptomatic after 20 hours. Thyroid surgery is unique to other day case procedures in that it is associated with a small but definite risk of life-threatening complications. Mortality incidence from population series are less than one per-cent [10] and [11] but the risk of death following a significant postoperative complication is unquantified. Reliability of more specific outcome data from complications is liable to publication bias, possibly more so in the day case setting where complications are notable by their however low incidence in some single centre series. Even in Tuggle’s state-wide review of over 1000 thyroidectomies [17] where the emergency room visit and re-admission rate of 7.8 and 2.3 per-cent respectively seem typical [13] and [16] the total bleed rate of under 0.2% is either a reflection of high volume surgeon performance or under-reporting. The three main risks of thyroid surgery are airway obstruction from haemorrhage/laryngeal oedema, vocal cord paresis and tetany from severe hypocalcaemia. This section will consider these in turn, along with recommendations to mitigate their occurrence and impact. When postoperative complications do occur, their recognition with prompt and effective management is critical.

The extract was filtered, pooled and concentrated on Rotavapour (Buchi, USA) and dried in lyophilizer RO4929097 (Laboconco, USA) under reduced pressure to obtain 10.6% of residue (CAEt). Preliminary qualitative phytochemical screening

of CAEt gave a positive result for steroids, carbohydrates, triterpenoids, resins, flavanoids, and tannins. Diabetes was induced in rats by injecting a freshly prepared solution of streptozotocin (STZ, 50 mg/kg bw, i.p) in 0.1 M citrate buffer, pH was 4.5. Fasting blood glucose concentration was measured after one week of STZ injection to confirm for induced diabetes. The rats with blood glucose level above 140 mg/dl were considered to be diabetic and were used in the experiment. The animals were kept fasting overnight for dosing as per experimental design. After induction of diabetes, forty rats were divided into five groups equally9 as follows. Group I: (control group): rats of this group received only vehicle solution. Fasting blood samples were drawn on 1st day after single administration of CAEt and after 7 and 14 days by tail vein puncture under mild ether anesthesia in Eppendroff’s tubes containing 50 ml of anticoagulant (10% trisodium citrate solution) from the normal and STZ-induced diabetic rats. All the animals were sacrificed by decapitation after recording the final body weight.

Blood was collected and serum was separated by centrifugation at 5000 rpm for 10 min for insulin assay by enzyme-linked selleck compound immunosorbent assay (ELISA) technique. After overnight fasting, on the day Megestrol Acetate the animals

were sacrificed, a zero-min blood sample was taken from tip of tail vein of all the rats: control (Group I), diabetic (Group II), CAEt (Group III), CAEt (Group IV) and tolbutamide (Group V). The rats of all groups were given glucose (2 g/kg) 30 min after dosing and blood samples were collected at 30th and 90th min for the measurement of glucose levels by single touch glucometer after the administration of glucose. Serum insulin was measured10 using ELISA kit from Boehringer Mannheim Diagnostic, Mannheim, Germany. The intra-assay variation was 4.9%. As the samples were run at a time there was no inter-assay variation. The insulin level in serum was expressed in μIU/ml. Lipid peroxidation in liver and kidney were estimated colorimetrically by thiobarbituric acid reactive substances (TBRAS)11 and hydroperoxides.12 Glutathione (GSH) was estimated using Beutler method,13 glutathione reductase (GSH-R) was estimated using the method of Horn.14 Superoxide dismutase (SOD) was measured by using Kakkar’s15 method. Catalase (CAT) activity was measured by using the rate of decomposition of H2O2 by method of Aebi.16 All these estimations were made in both liver and kidney. Total cholesterol (TC), high density lipoproteins (HDL) cholesterol, Triglyceride (TG) levels in serum were measured spectrophometrically by Allian Buccolo method.17 Low-density lipoprotein (LDL) cholesterol was calculated by Friedewald’s method.

This was a randomized, open-label, multicenter trial in 550 children aged 12 to 18 months in Taiwan. All children received one dose of JE-CV and one dose of MMR vaccine either separately or concomitantly. Children were randomly

allocated (1:2:2 ratio) to one of three groups (JE-CV, MMR or Co-Ad). The JE-CV Group received JE-CV followed by MMR 6 weeks later. The MMR Group received MMR followed by JE-CV 6 weeks later. The Co-Ad Group received both vaccines at the same visit (Fig. 1). The study was performed in accordance with the Declaration of Helsinki, Good Clinical Practice, International Conference on Harmonization, the European Directive 2001/20/EC and applicable national and local requirements. It was approved by the Institutional Review Board of each study center, and the Department of Health Ethics Committee. Paclitaxel concentration Written informed consent was obtained from at least one parent or legally acceptable representative. Healthy children with normal birth weight were enrolled. Exclusion criteria included previous vaccination against

JE, measles, mumps or rubella, contraindication to any vaccine-related component, receipt of any other vaccination within 4 weeks preceding the study or planned within 6 weeks following the study, receipt of blood within 6 months before the study, receipt of plasma within 11 months before the study, or participation in any other interventional trial. The study was carried out at five sites in Taiwan: National Taiwan University Hospital, Volasertib Taipei; Chang Gung Children’s Hospital, Taoyuan; Mackey Memorial Hospital, Taipei; Taichung Veterans General Hospital, Taichung; and Far Eastern Memorial Hospital,

New Taipei City. There were seven visits for JE-CV and MMR Groups: Day (D)0, D28, D42, D70, D84, Month (M)6 and M12; and five visits for children in Co-Ad Group: D0, D28, D42, M6 and M12. The M6 visit was 6 months after the last vaccination, and the M12 visit was 12 months after the aminophylline first vaccination. Both vaccines were administered subcutaneously; JE-CV into the thigh, the MMR vaccine into the upper arm. Blood samples were collected from children in JE-CV and MMR Groups on D0, D42, D84, M6 and M12, and from children in Co-Ad Group on D0, D42, M6 and M12 (Fig. 1). Treatment allocation was done using an interactive voice response system (IVRS). Randomization was done using the permuted block method with stratification on study center. The vaccinator took one dose corresponding to the group assigned by the IVRS. Each dose had a unique number. The child’s parent/guardian was provided with a diary card to record information about solicited injection site and systemic reactions up to 7 and 14 days after each vaccination, respectively, and record information about unsolicited adverse events (AE)s up to 28 days after each vaccination.

Fraction IV (300 mg) was chromatographed on a Sephadex LH-20 column using CH3CN–H2O (9:1) as eluent to give the compound 7 (70 mg). Amorphous powder, [α]D25 + 127.7° (c 0.5, MeOH); IR(KBr) νmax: 3405, 2932, 1705, 1273, 1176, 1073; 1H NMR (300 MHz, CD3OD): δ 7.36 (1H, s, H-3), 5.56 (1H, d, J = 3.8 Hz, H1), 4.63 (1H, d, J = 7.7 Hz, H-1), 3.91 (1H, dd, J = 5.3 and1.3 Hz, H-7), 3.72–3.26 (4H, m), 3.69 (3H, s, COOMe), 3.30 (2H, m) 3.20 (1H, m), 2.63 (1H, d, J = 8. 6 Hz, H-9), 2.20 (1H, m), 1.73 (1H, m), 1.31 (3H, s, H-10). 13C NMR (75 MHz,

CD3OD): δ 168.6, 151.0,

113.6, 99.3, 94.5, 79.7, 78.8, 78.4, 78.0, 77.5, 73.9, 70.9, 62.5, 51.8, 38.4, SKI-606 cost 26.9, 21.8. ESIMS: m/z 429 (M + Na)+. Amorphous powder, [α]D25 + 41.0° (c 0.5, MeOH); IR(KBr) νmax: 3421, 1702, 1634, 1524, 1445, 1288, 1172, 1075, 865, 765 cm −1; 1H NMR (300 MHz, CD3OD): δ 7.79 (1H, d, J = 15.8 Hz, H-7″), 7.41 (1H, d, J = 1.8 Hz, Vorinostat manufacturer H-2″), 7.31 (1H, s, H-3), 6.98 (2H, m), 6.54 (1H, d, J = 15.8 Hz, H-8″), 5.80 (1H, d, J = 3.9 Hz, H-1), 4.85 (1H, dd, J = 5.3 and1.7 Hz, H-7), 4.63 (1H, d, J = 7.74 Hz, H-1′), 3.86 (3H, s, OMe), 3.79 (3H, s, COOMe), 3.69 (1H, dd, J = 11.6 and 5.6 Hz, H-6′), 3.37–3.29 (4H, m), 2.91 (1H, d, J = 8. 9 Hz, H-9), 2.43 (m, 2H), 1.13 (3H, s, H3-10). 13C NMR (75 MHz, CD3OD): δ 168.6, 167.4, 152.3, 151.2, 150.9, 146.5, 145.3, 130.3, 129.8, 128.8, 128.1, 117.8, 99.7, 94.3, 79.8, 78.8, 78.5, 77.5, 76.5, 72.6, 70.9, 62.3, 57.6, 55.1, 51.7, 45.6,

21.7. Amorphous powder, [α]D25 + 41.6° (c 0.5, MeOH); IR(KBr) νmax: 3420, 1705, 1634, 1514, 1445, 1285, 1170, 1075, 868, 765 cm −1; 1H NMR (300 MHz, CD3OD): δ 7.78 (1H, d, J = 15.8 Hz, H-7″), 7.39 (1H, d, J = 1.7 Hz, H-2″), 7.31 (1H, s, H-3), 6.98 (2H, m), 6.53 (1H, d, J = 15.8 Hz, H-8″), 5.80 (1H, d, J = 4.0 Hz, H-1), 4.85 (1H, dd, J = 5.3 and 1.8 Hz, H-7), 4.63 (1H, d, J = 7.74 Hz, Adenosine H-1′), 3.90 (3H, s, OMe), 3.86 (3H, s, OMe), 3.79 (3H, s, COOMe), 3.69 (1H, dd, J = 11.6 and 5.6 Hz, H-6′), 3.37–3.29 (4H, m), 2.93 (1H, d, J = 8.7 Hz, H-9), 2.43 (2H m), 1.17 (3H, s, H3-10).