T2DM may exert a protective effect against digestive system tumors in East Asian populations: a Mendelian randomization analysis.

Introduction: Type 2 diabetes mellitus (T2DM) was associated with digestive system tumors. We analyzed publicly available data from GWAS studies using Mendelian randomization methods to clarify its causal relationship and mechanisms. Five common digestive system tumors and four diabetes-related phenotypes were included. Methods: Inverse variance weighted method was the main analytical method. Meta-analysis was used to summarize results of multiple data sources. Horizontal pleiotropy was tested using Egger-intercept method and validated by MRPRESSO method. Heterogeneity and sensitivity analysis were conducted by Cochran's Q test and leave-one-out method, respectively. Results: T2DM is associated with a reduced risk of esophageal (OR: 0.77, 95% CI: 0.71 to 0.83, P< 0.001), gastric (OR: 0.87, 95% CI: 0.84 to 0.90, P< 0.001) and colorectal cancer (OR: 0.88, 95% CI: 0.85 to 0.91, P< 0.001) and hepatocellular carcinoma (OR: 0.92, 95% CI: 0.86 to 0.97, P = 0.005) and an increased risk of pancreatic cancer (OR: 1.92, 95% CI: 1.47 to 2.50, P< 0.001) in East Asian population. T2DM causes decreased fasting insulin levels (OR = 0.966, 95% CI: 0.95 to 0.98, P< 0.001) and increased glycated hemoglobin levels (OR=1.41, 95% CI: 1.39 to 1.44, P<0.001). Elevated fasting insulin levels increase the risk of esophageal cancer (OR = 10.35, 95% CI: 1.10 to 97.25, P = 0.041), while increased glycated hemoglobin levels increase pancreatic cancer risk (OR=2.33, 95% CI: 1.37 to 3.97, P=0.002) but decrease gastric cancer risk (OR=0.801, 95% CI: 0.65 to 0.99, P=0.044). Conclusion: T2DM is associated with a reduced risk of esophageal, gastric and colorectal cancer and hepatocellular carcinoma in East Asian populations. The causal relationships between T2DM with esophageal and gastric cancer are partially mediated by decreased fasting insulin and increased glycated hemoglobin levels, respectively. T2DM indirectly increases the risk of pancreatic cancer by increasing glycated hemoglobin levels.

Transplantation of Wnt5a-modified Bone Marrow Mesenchymal Stem Cells Promotes Recovery After Spinal Cord Injury via the PI3K/AKT Pathway.

Spinal cord injury (SCI) is a severe neurological condition that can lead to paralysis or even death. This study explored the potential benefits of bone marrow mesenchymal stem cell (BMSC) transplantation for repairing SCI. BMSCs also differentiate into astrocytes within damaged spinal cord tissues hindering the cell transplantation efficacy, therefore it is crucial to enhance their neuronal differentiation rate to facilitate spinal cord repair. Wnt5a, an upstream protein in the non-classical Wnt signaling pathway, has been implicated in stem cell migration, differentiation, and neurite formation but its role in the neuronal differentiation of BMSCs remains unclear. Thus, this study investigated the role and underlying mechanisms of Wnt5a in promoting neuronal differentiation of BMSCs both in vivo and in vitro. Wnt5a enhanced neuronal differentiation of BMSCs in vitro while reducing astrocyte differentiation. Additionally, high-throughput RNA sequencing revealed a correlation between Wnt5a and phosphoinositide 3-kinase (PI3K)/protein kinase B(AKT) signaling, which was confirmed by the use of the PI3K inhibitor LY294002 to reverse the effects of Wnt5a on BMSC neuronal differentiation. Furthermore, transplantation of Wnt5a-modified BMSCs into SCI rats effectively improved the histomorphology (Hematoxylin and eosin [H&E], Nissl and Luxol Fast Blue [LFB] staining), motor function scores (Footprint test and Basso-Beattie-Bresnahan [BBB]scores)and promoted neuron production, axonal formation, and remodeling of myelin sheaths (microtubule associated protein-2 [MAP-2], growth-associated protein 43 [GAP43], myelin basic protein [MBP]), while reducing astrocyte production (glial fibrillary acidic protein [GFAP]). Therefore, targeting the Wnt5a/PI3K/AKT pathway could enhance BMSC transplantation for SCI treatment.

Di-2-ethylhexyl phthalate affects zinc metabolism and neurogenesis in the developing rat brain.

We previously observed that developmental marginal zinc deficiency affects neurogenesis. Maternal phthalate exposure could disrupt fetal zinc homeostasis by triggering an acute phase response, causing maternal liver zinc retention that limits zinc availability to the fetus. Thus, we currently investigated whether exposure to di-2-ethylhexyl phthalate (DEHP) during gestation in rats alters fetal brain neurogenesis by impairing zinc homeostasis. Dams consumed an adequate (25 µg zinc/g diet) (C) or a marginal zinc deficient (MZD) (10 µg zinc/g diet) diet, without or with DEHP (300 mg/kg BW) (C + DEHP, MZD + DEHP) from embryonic day (E) 0 to E19. To evaluate neurogenesis we measured parameters of neural progenitor cells (NPC) proliferation and differentiation. Maternal exposure to DEHP and/or zinc deficiency lowered fetal brain cortical tissue (CT) zinc concentrations. Transcription factors involved in NPC proliferation (PAX6, SOX2, EMX1), differentiation (TBR2, TBR1) and mature neurons (NeuN) were lower in MZD, MZD + DEHP and C + DEHP than in C E19 brain CT, being the lowest in the MZD + DEHP group. VGLUT1 levels, a marker of glutamatergic neurons, showed a similar pattern. Levels of a marker of GABAergic neurons, GAD65, did not vary among groups. Phosphorylated ERK1/2 levels were reduced by both MZD and DEHP, and particularly in the MZD + DEHP group. MEHP-treated human neuroblastoma IMR-32 cells and E19 brains from DEHP-treated dams showed that the zinc-regulated phosphatase PP2A can be in part responsible for DEHP-mediated ERK1/2 downregulation and impaired neurogenesis. Overall, gestational exposure to DEHP caused secondary zinc deficiency and impaired neurogenesis. These harmful effects could have long-term consequences on the adult offspring brain structure and function.

Endolymphatic Hydrop Phenotype in Familial Norrie Disease Caused by Large Fragment Deletion of NDP.

Norrie disease (ND; OMIM 310600), a rare X-linked recessive genetic disorder, is characterized by congenital blindness and occasionally, sensorineural hearing loss, and developmental delay. The congenital blindness of ND patients is almost untreatable; thus, hearing is particularly important for them. However, the mechanism of hearing loss of ND patients is unclear, and no good treatment is available except wearing hearing-aid. Therefore, revealing the mechanism of hearing loss in ND patients and exploring effective treatment methods are greatly important. In addition, as a serious monogenic genetic disease, convenient gene identification method is important for ND patients and their family members, as well as prenatal diagnosis and preimplantation genetic diagnosis to block intergenerational transmission of pathogenic genes. In this study, a Norrie family with two male patients was reported. This pedigree was ND caused by large fragment deletion of NDP (norrin cystine knot growth factor NDP) gene. In addition to typical severe ophthalmologic and audiologic defects, the patients showed new pathological features of endolymphatic hydrops (EH), and they also showed acoustic nerves abnormal as described in a very recent report. PCR methods were developed to analyze and diagnose the variation of the family members. This study expands the understanding of the clinical manifestation and pathogenesis of ND and provides a new idea for the treatment of patients in this family and a convenient method for the genetic screen for this ND family.

A Novel missense mutation of COL2A1 gene in a large family with stickler syndrome type I.

Stickler syndrome type I (STL1, MIM 108300) is characterized by ocular, auditory, skeletal and orofacial manifestations. Nonsyndromic ocular STL1 (MIM 609508) characterized by predominantly ocular features is a subgroup of STL1, and it is inherited in an autosomal dominant manner. In this study, a novel variant c.T100>C (p.Cys34Arg) in COL2A1 related to a large nonsyndromic ocular STL1 family was identified through Exome sequencing (ES). Bioinformatics analysis indicated that the variant site was highly conserved and the pathogenic mechanism of this variant may involve in affected structure of chordin-like cysteine-rich (CR) repeats of ColIIA. Minigene assay indicated that this variant did not change alternative splicing of exon2 of COL2A1. Moreover, the nonsyndromic ocular STL1 family with 16 affected members showed phenotype variability and certain male gender trend. None of the family members had hearing loss. Our findings would expand the knowledge of the COL2A1 mutation spectrum, and phenotype variability associated with nonsyndromic ocular STL1. Search for genetic modifiers and related molecular pathways leading to the phenotype variation warrants further studies.

Role of Endoplasmic Reticulum Stress in Otitis Media.

Endoplasmic reticulum (ER) stress occurs in many inflammatory responses. Here, we investigated the role of ER stress and its associated apoptosis in otitis media (OM) to elucidate the mechanisms of OM and the signaling crosstalk between ER stress and other cell damage pathways, including inflammatory cytokines and apoptosis. We examined the expression of inflammatory cytokine- and ER stress-related genes by qRT-PCR, Western blotting, and immunohistochemistry (IHC) in the middle ear of C57BL/6J mice after challenge with peptidoglycan polysaccharide (PGPS), an agent inducing OM. We also evaluated the effect of the suppression of ER stress with tauroursodeoxycholic acid (TUDCA), an ER stress inhibitor. The study revealed the upregulation of ER stress- and apoptosis-related gene expression after the PGPS treatment, specifically ATF6, CHOP, BIP, caspase-12, and caspase-3. TUDCA treatment of PGPS-treated mice decreased OM; reduced the expression of CHOP, BIP, and caspase 3; and significantly decreased the proinflammatory gene expression of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). These results suggest that PGPS triggers ER stress and downstream proinflammatory gene expression in OM and that inhibition of ER stress alleviates OM. We propose that ER stress plays a critical role in inflammation and cell death, leading to the development of OM and points to ER stress inhibition as a potential therapeutic approach for the prevention of OM.

Correlation between the rs7101 and rs1063169 polymorphisms in the FOS noncoding region and susceptibility to and prognosis of colorectal cancer.

BACKGROUND: The FOS gene is located on human chromosome 14q21-31 and encodes the nuclear oncoprotein c-Fos. This study analyzed the correlation between the FOS noncoding region rs7101 and rs1063169 polymorphisms and colorectal cancer susceptibility and prognosis. METHODS: We analyzed the FOS genotypes in 432 colorectal cancer patients and 315 healthy subjects by PCR/Sanger sequencing. Survival was analyzed by Kaplan-Meier and Cox regression analysis. Western blot was used to detect the expression of c-Fos protein in cancer tissues and adjacent tissues in colorectal cancer patients with different genotypes. RESULTS: The presence of a T allele at rs7101 and a T allele at rs1063169 in FOS carried a higher risk of colorectal cancer [adjusted odds ratio (OR) = 1.237, 95% confidence interval (95% CI) = 1.131-1.346, P ≤ .001 and adjusted OR = 1.218, 95% CI = 1.111-1.327, P ≤ .001, respectively]. c-Fos protein levels were significantly higher in variant cancer tissues than in normal mucosa tissues (P < .05), and c-Fos proteins levels were also higher in homozygous variant cancer tissues than in heterozygous variant cancer tissues. The 3-year survival rate of patients with wild-type FOS was higher than that of patients with variant FOS (P < .05). CONCLUSION: The rs7101 and rs1063169 polymorphisms in the noncoding region of FOS are associated with the risk of developing colorectal cancer and the progression of colorectal cancer, which may be because the mutation enhances the expression of c-Fos protein to promote the incidence and development of colorectal cancer.

Analysis of the expression of D-dimer, CD147 and miR203 and their correlation in gastric cancer.

OBJECTIVES: To evaluate the relationship of D-dimer, CD147 and miR-203, and detect the influence of these biomarkers on the pathological characteristics in patients with gastric cancer. METHODS: The patients with gastric cancer treated using radical gastrectomy between May 2013 and October 2017 were reviewed retrospectively. The expression of D-dimer, miR203 and CD147 was measured for all the patients, and the clinical data including age, gender, tumor size, tumor differentiation, invasion depth, lymphatic metastasis, TMN stage, and pathological type were retrieved and analyzed. The study was carried out in affiliated Yidu Central Hospital of Weifang Medical College, Qingzhou, China. RESULTS: Two hundred sixty patients with gastric cancer were included. The patients with tumor metastasis, larger tumor diameter, lower differentiation, lymphatic metastasis, deeper invasion, and higher TMN stage presented with a significantly higher D-dimer and CD 147 expression, but the level of the two biomarkers didn't show a significant difference in patients with different pathological type, gender and age. Compared with CD147 and D-dimer, miR203 presented with different characteristics of expression. In addition, the expression of miR203 was negatively correlated with CD147 and D-dimer, and there was a positive correlation between CD147 and D-dimer in patients with gastric cancer. CONCLUSION: In this study, a close correlation of D-dimer, miR203 and CD147 was found, and these three biomarkers should be screened in gastric cancer patients.

Sirt6 regulates efficiency of mouse somatic reprogramming and maintenance of pluripotency.

BACKGROUND: Mouse somatic cells can be reprogrammed into induced pluripotent stem cells (iPSCs) by defined factors known to regulate pluripotency, including Oct4, Sox2, Klf4, and c-Myc. It has been reported that Sirtuin 6 (Sirt6), a member of the sirtuin family of NAD+-dependent protein deacetylases, is involved in embryonic stem cell differentiation. However, whether and how Sirt6 influences epigenetic reprogramming remains unknown. METHODS: Mouse embryonic fibroblasts isolated from transgenic Oct4-GFP reporter mice with or without Sirt6 were used for reprogramming by Yamanaka factors. Alkaline phosphatase-positive and OCT4-GFP-positive colony were counted to calculate reprogramming efficiency. OP9 feeder cell co-culture system was used to measure the hematopoietic differentiation from mouse ES and iPS cells. RNA sequencing was measured to identify the differential expressed genes due to loss of Sirt6 in somatic and pluripotent cells. RESULTS: In this study, we provide evidence that Sirt6 is involved in mouse somatic reprogramming. We found that loss of function of Sirt6 could significantly decrease reprogramming efficiency. Furthermore, we showed that Sirt6-null iPS-like cell line has intrinsically a differentiation defect even though the establishment of normal self-renewal. Particularly, by performing transcriptome analysis, we observed that several pluripotent transcriptional factors increase in knockout cell line, which explains the underlying loss of pluripotency in Sirt6-null iPS-like cell line. CONCLUSIONS: Taken together, we have identified a new regulatory role of Sirt6 in reprogramming and maintenance of pluripotency.

Distribution characteristics of different human papillomavirus genotypes in women in Wuhan, China.

BACKGROUND: Human papillomaviruses (HPVs) are strongly associated with the development of cervical carcinoma, and the distribution of HPV genotypes varies regionally. METHODS: To investigate the distribution characteristics of different genotypes of HPV infection in women in Wuhan, China, a total of 13 775 patients were enrolled over 2 years. RESULTS: Of these, 2436 patients were infected with HPVs, and the total infection rate was 17.68%. The infection rate of high-risk HPV (HR-HPV) was significantly higher (13.96%) than that of single low-risk HPV (LR-HPV; 3.72%). Among the HR-HPV infections, the most common genotype was HPV 52 with an infection rate of 4.23%, followed by HPVs 16, 58, 39, and 51. The most common LR-HPV genotype was HPV 81, followed by HPVs 6, 11, and 44. Patients under the age of 25 years were found to have the highest HPV infection rate (P < .05). After the age range of 51-55 years, a downward trend in total HPVs and HR-HPVs was observed. The HPV infection rate for a single genotype was higher than that for multiple HPVs (P < .01), and the detection rates in summer and winter were significantly higher than those in spring and autumn. CONCLUSIONS: The results demonstrate that the distribution characteristics of various HPV genotype infections are associated with region and age and may be related to season. These data could be the basis for further epidemiological analysis into the control and prevention of HPV infection in this region.

Curcumin and its promise as an anticancer drug: An analysis of its anticancer and antifungal effects in cancer and associated complications from invasive fungal infections.

Invasive fungal infections (IFI) are important complications of cancer, and they have become a major cause of morbidity and mortality in cancer patients. Effective anti-infection therapy is necessary to inhibit significant deterioration from these infections. However, they are difficult to treat, and increasing antifungal drug resistance often leads to a relapse. Curcumin, a natural component that is isolated from the rhizome of Curcuma longa plants, has attracted great interest among many scientists studying solid cancers over the last half century. Interestingly, curcumin provides an ideal alternative to current therapies because of its relatively safe profile, even at high doses. To date, curcumin's potent antifungal activity against different strains of Candida, Cryptococcus, Aspergillus, Trichosporon and Paracoccidioides have been reported, indicating that curcumin anticancer drugs may also possess an antifungal role, helping cancer patients to resist IFI complications. The aim of this review is to discuss curcumin's dual pharmacological activities regarding its applications as a natural anticancer and antifungal agent. These dual pharmacological activities are expected to lead to clinical trials and to improve infection survival among cancer patients.

The role of the vascular endothelial growth factor/vascular endothelial growth factor receptors axis mediated angiogenesis in curcumin-loaded nanostructured lipid carriers induced human HepG2 cells apoptosis.

BACKGROUND: Curcumin (diferuloylmethane), the active constituent of turmeric extract has potent anti-cancer properties have been demonstrated in hepatocellular carcinoma (HCC). However, its underlying molecular mechanism of therapeutic effects remains unclear. Vascular endothelial growth factor (VEGF) and its receptors (VEGFRs) have crucial roles in tumor angiogenesis. PURPOSE: The goal of this study was to investigate the role of the VEGF/VEGFRs mediated angiogenesis during the proliferation and apoptosis of human HepG2 hepatoma cell line and the effect of curcumin-loaded nanostructured lipid carriers (Cur-NLC). MATERIALS AND METHODS: The proliferation of HepG2 cells was determined by methyl thiazolyl tetrazolium after exposure to Cur-NLC and native curcumin. Apoptosis was quantified by flow cytometry with annexin V-fluorescein isothiocyanate and propidium iodide staining. Cellular internalization of Cur-NLC was observed by fluorescent microscope. The level of VEGF was detected by enzyme-linked immunosorbent assay kits. The expression of VEGFRs was quantified by Western blotting. RESULTS: Cur-NLC was more effective in inhibiting the proliferation and enhancing the apoptosis of HepG2 cells than native curcumin. Fluorescent microscope analysis showed that HepG2 cells internalized Cur-NLC more effectively than native curcumin. Furthermore, Cur-NLC down-regulated the level of VEGF and the expression of VEGFR-2, but had a slight effect on VEGFR-1. CONCLUSION: These results clearly demonstrated that Cur-NLC was more effective in anti-cancer activity than the free form of curcumin. These studies demonstrate for the 1 st time that Cur-NLC exerts an antitumor effect on HepG2 cells by modulating VEGF/VEGFRs signaling pathway.

[Comparison of three different bone grafts for spinal fusion of degenerative lumbar disease].

OBJECTIVE: To compare the effectiveness of three different bone grafts [autogenous bone, allogeneic bone, and bone morphogenetic protein (BMP) composite bone] combined with screw system for spinal fusion of degenerative lumbar disease. METHODS: Between January 2005 and January 2010, 102 cases of degenerative lumbar disease were randomly treated with autogenous bone (group A, n=35), allogeneic bone (group B, n=33), and BMP composite bone (group C, n=34). There was no significant difference in sex, age, disease duration, affected segments, Meyerding grade, preoperative intervertebral space height, and the Japanese Orthopaedic Association (JOA) score among 3 groups (P > 0.05). The intervertebral space height, bone fusion rate, and JOA score were compared among 3 groups at different time points. RESULTS: All patients of 3 groups were followed up 2 to 5 years, with an average of 3.2 years. At 6 to 24 months after operation, the intervertebral space height significantly increased when compared with preoperative value in 3 groups (P < 0.05); the intervertebral space height of groups A and C was significantly greater than that of group B at 6, 12, 18, and 24 months after operation (P < 0.05), but no significant difference was found between groups A and C (P > 0.05). Bone graft fusion was observed at 6 months in groups A and C and at 12 months in group B; at 24 months, the rate of bone graft fusion was 100% in groups A and C, and 87.88% in group B, showing significant difference (P < 0.05). There was significant difference in JOA score between preoperation and postoperative 12th and 24th months (P < 0.05); at 12 and 24 months after operation, JOA socre and improving rate of groups A and C were significantly higher than those of group B (P < 0.05), but no significant difference was found between groups A and C (P > 0.05). CONCLUSION: The effect of BMP composite bone is equivalent to that of autogenous bone graft in treating spinal fusion of degenerative lumbar disease, and they are better than allogeneic bone graft. BMP composite bone can obtain adequate bone grafts without invasive sampling, and has fast fusion and high successful rate.

Antitumor and immunomodulatory activity of arabinoxylans: a major constituent of wheat bran.

We aimed to investigate the antitumor activity of wheat bran arabinoxylans, including the role of its immunostimulatory effect. In S180 tumor-bearing mice arabinoxylan administration significantly inhibited the growth of mouse transplantable tumors and remarkably promoted thymus and spleen indexes, splenocyte proliferation, natural killer cell and macrophage phagocytosis activity, interleukin 2 production, and delayed-type hypersensitivity reaction. In addition, it increased peripheral leukocyte count, and bone-marrow cellularity in tumor-bearing mice. As the antitumor activity of arabinoxylans may be mediated via the improvement in the immune response, they can be considered an antitumor agent with immunomodulatory activity.

[The measurement of radiation dosage in diagnostic x-ray device].

In order to improve the diagnostic quality of X-ray device and to promote the implementation of radiation protection in accordance to the ICRU definition and ICRP classification standards for measuring radiation harm to human body, we have made a number of tests, including the kinetic energy released by ionizing air, the Half-value layer, the output dose coincidence, the High contrast resolution, the Consistency between visual light field and project X-ray field, and the Focus of X-ray tube. We have also analysed the measured data and results. The tests were conducted on the XEB150L-20 made by Shimadzu Co. in the middle of 1990s.

[Effect of vitrification state of protective solutions on recovery of red blood cells after lyophilization preservation].

To study effect of vitrification state of protective solutions on recovery of red blood cells after lyophilization, four protective solutions composed of isotonic buffers containing 7% DMSO (v/v) and 20%, 30%, 40% or 50% polyvinylpyrrolidone (PVP) (w/v) were adopted. Vitrification state of protective solutions was examined first when white ice crystal appeared in any protective solution during freezing or thawing, if the used solution was not a vitrification solution. Red blood cells were lyophilized in MINILYO45 freeze-dryer after washing, mixing with protective solutions and prefreezing. After lyophilization, the samples were quickly rehydrated by 37 degrees C rehydration solution. The results showed that in vitrification and devitrification experiments, white ice crystal appeared in solution of 20% PVP + 7% DMSO and 30% PVP + 7% DMSO during freezing and thawing; vitrification appeared in solution of 40% PVP + 7% DMSO during freezing, but devitrification appeared during thawing; vitrification appeared in solution of 50% PVP + 7% DMSO during freezing and thawing. After rehydration, the recoveries of red blood cells and hemoglobin in 40% PVP + 7% DMSO group were (81.36 +/- 14.94)% and (77.54 +/- 12.86)%, which were significantly higher than that in 20% PVP + 7% DMSO, 30% PVP + 7% DMSO and 50% PVP + 7% DMSO groups (P < 0.01). The concentration of free hemoglobin in 40% PVP + 7% DMSO group was also significantly lower than that in other three groups (P < 0.01). With increase of PVP concentration in protective solutions, vitrification state and protective effect of these solutions also increased; when concentration of PVP in protective solution was 40% though it was not a vitrification solution, the effect of lyophilization was the best; but when concentration of PVP further increased to 50%, though it was a vitrification solution, the effect decreased. It is concluded that excessive vitrification state could not benefit lyophilization of red blood cells.

[Therapeutic Effects of rhIL-11 on Carboplatin-Induced Thrombocytopenia in Monkeys]

A model of myelosuppression with thrombocytopenia was produced in monkey by i.v. administration of carboplatin to the evaluate effects of rhIL-11 treatment in monkeys. Following myelosuppression, rhIL-11 was subcutaneously injected for 19 consecutive days at the dose of 50 or 100 micro g/kg. In myelosuppressed monkeys treated with rhIL-11, peripheral blood platelet started to drop at the day 8 after the administration of carboplatin, and reaching the nadir between the day 12 - 14, the decrease in blood platelet was less severe compared with untreated monkeys; peripheral blood platelet began to recovery on day 11 - 13 (D14 - D16) after rhIL-11 treatment, and reached or surpassed the baseline value before carboplatin administration after 13 - 15 days rhIL-11 treatment. Blood platelet counts remained high level after discontinuation of rhIL-11 administration and returned to baseline after 4 days. The results demonstrated that rhIL-11 has a significant thrombopoietic activity, it can reduce the severity of thrombocytopenia as well as shorten the duration of thrombocytopenia caused by myeloablastive agents, and is likely to become an effective agent against thrombocytopenia induced by chemotherapy.