Rare cytochalasans isolated from the mangrove endophytic fungus Xylaria arbuscula.

Four new cytochalasans, arbuschalasins A-D (1-4), along with thirteen known analogues (5-17), were isolated from the solid rice medium of endophytic fungus Xylaria arbuscula. Arbuschalasins A-B feature a rare 5/6/6/6 fused ring system while arbuschalasin D was characterized as the first example of natural cytochalasans that possesses a 5/5/11 fused scaffold. The structures of 1-4 were assigned by spectroscopic data, with their absolute structures being determined by electronic circular dichroism (ECD) calculations. All of the isolates were evaluated against the human colorectal adenocarcinoma cell lines (HCT15). Compounds 6 and 7 showed significant inhibitory effects (IC50 values were 13.5 and 13.4 µM, respectively), being more active than those of the positive control, fluorouracil (103.1 µM).

Quassinoids from the Roots of Eurycoma longifolia and Their Anti-Proliferation Activities.

A phytochemical investigation on the roots of medicinal plant Eurycoma longifolia resulted in the isolation of 10 new highly oxygenated C20 quassinoids longifolactones G‒P (1-10), along with four known ones (11-14). Their chemical structures and absolute configurations were unambiguously elucidated on the basis of comprehensive spectroscopic analysis and X-ray crystallographic data. Notably, compound 1 is a rare pentacyclic C20 quassinoid featuring a densely functionalized 2,5-dioxatricyclo[5.2.2.04,8]undecane core. Compound 4 represents the first example of quassinoids containing a 14,15-epoxy functionality, and 7 features an unusual α-oriented hydroxyl group at C-14. All isolated compounds were evaluated for their anti-proliferation activities on human leukemia cells. Among the isolates, compounds 5, 12, 13, and 14 potently inhibited the in vitro proliferation of K562 and HL-60 cells with IC50 values ranging from 2.90 to 8.20 µM.

[Morinda Officinalis How improves cellphone radiation-induced abnormality of LH and LHR in male rats].

OBJECTIVE: To investigate the effects of Morina Officinalis How (MOH) on the abnormal levels of serum luteotrophic hormone (LH) and LH receptor (LHR) in the testis tissue induced by cellphone radiation (CPR) in rats. METHODS: Fifty adult male SD rats were randomly divided into five groups of equal number: sham CPR, untreated CPR, negative double distilled water (DDW) control, aqueous MOH extract, and alcohol MOH extract. All the animals were exposed to mobile phone radiation except those of the sham CPR group. Then, the rats of the latter two groups were treated intragastrically with MOH at 20 g per kg of the body weight per day in water and alcohol, respectively. After 2. weeks of treatment, all the rats were sacrificed for measurement of the levels of serum LH and LHR in the testis tissue. RESULTS: The levels of serum LH and LHR were 30.15 ± 8.71 and 33.28 ± 6.61 in the aqueous MOH group and 0.96 ± 0.06 and 0.94 ± 0.08 in the alcohol MOH group, both significantly decreased as compared with the negative DDW controls (P < 0.05), but with no remarkable difference between the two MOH groups (P > 0.05). CONCLUSION: MOH can improve CPR-induced abnormality of LH and LHR in adult male rats.

[Clinical significance of sequential monitoring minimal residual disease in childhood B-cell acute lymphoblastic leukemia].

OBJECTIVE: To study the clinical significance of sequentially monitoring minimal residual disease (MRD) in childhood B-cell acute lymphoblastic leukemia (B-ALL). METHOD: Eighty one B-ALL cases were enrolled in the study from January 2004 to December 2009. Leukemia cell markers were detected by flow cytometry at diagnosis, then regularly followed-up. RESULTS: Of 81 cases, 80 achieved complete remission (CR) after induction therapy, 5-year event-free survival (EFS) was (76.80 ± 5.70)%. Among them, the EFS was (89.40 ± 5.90)% in standard risk group and (66.99 ± 13.60)% in intermediate risk group. Eight cases were screened for leukemia markers for MRD monitoring and identified in 68; and 5-year EFS was (79.10 ± 6.20)% and (62.50 ± 15.10)% (P > 0.05, respectively). MRD detection at day 35 in induction therapy showed that 52 of 68 cases were MRD negative (leukemia cells < 0.01%), the 5-year EFS being (88.50 ± 4.90)%, and 16 were MRD positive (leukemia cells ≥ 0.01%), the 5-year EFS being (42.10 ± 20.10)% (P > 0.05). Univariate analysis confirmed that there was a correlation between MRD monitoring and risk stratification. MRD detection at day 55 showed that among the 52 day 35 MRD negative cases, 51 were still negative, 1 positive, among 16 day 35 MRD positive cases, 14 (87.50%) turned negative, 2 still positive. Of the 68 cases, 9 were MRD positive within one year after CR (3 relapsed), 4 MRD positive after one year (2 relapsed) and 55 MRD negative (4 relapsed) (P > 0.05). CONCLUSIONS: Sequential monitoring MRD can find out treatment outcome and adjust therapy in time.

[Expression and significance of P57(kip2) and Maspin in pathological scar].

OBJECTIVE: To study the expression of P57(kip2) and Maspin in the pathological scar and their possible role in the pathogenesis of abnormal scars. METHODS: Immunohistochemistry integrated image analysis and reverse transcription polymerase chain reaction (RT-RCR) were performed to detect the expression of P57(kip2) and Maspin in hypertrophic scar, keloid, mature scar and normal skin. Statistics was used to analyze the datas. RESULTS: The expression of P57(kip2) protein was fixed to fibroblast intranuclear in abnormal scar, and the expression of P57(kip2) protein and P57(kip2) mRNA decreased (P < 0.05). The expression of Maspin protein was fixed to fibroblast cytoplasm and intranuclear in abnormal scar, and the expression of Maspin protein and Maspin mRNA decrease, compared with that in normal group (P < 0.05). There was positive correlation between P57(kip2) protein and Maspin protein expression (P < 0.01). CONCLUSIONS: The decreased expression of P57(kip2) and Maspin in abnormal scar shows that they are cicatrix-related genes. There is a positive relationship between the two genes. It may be one of the mechanisms of pathogenesis of abnormal scar. It makes effect through fibroblasts.