Objective To explore the causes of dengue fever resurgence in Guangxi, and to analyze the risk factors of dengue fever. Methods The descriptive epidemiological analysis was conduced based on the dengue fever data reported from 2006 to 2015, and the surveillance results of aedes and antibody levels in health population from 2013 to 2015 in Guangxi. Results Before 2013, dengue fever was imported from foreign country in Guangxi, accounting for 95.35％(42/45), and 75.71％of the imported cases was imported from Southeast Asia. The local outbreak of dengue fever was happened in 2014, accounted for 94.02％(849/903) of the total number of 10 years. From onset to diagnosis, Guangxi dengue fever cases need 0-70 d (median time interval is 6 d). Cases were reported year-round, but the peak season for the onset of dengue fever was from September to November, accounting for 96.46％of all cases (871/903). The number of cases reported in Nanning was the most (83.37％), followed by Wuzhou city (7.44％) and Guilin city (4.81％), and all the three cities had dengue fever outbreaks. The cases were mainly commercial service staff (27.80％) and houseworkers and unemployed people (18.16％). Results of aedes monitoring showed that the density of aedes was high in Guangxi. In more than 50％ of the monitoring seasons the breteau index (BI) stayed greater than 20. However, the antibody positive rate was only 3％ in the healthy residents of Guangxi. Conclusion The risk of dengue fever is high in Guangxi. Therefore, it is essential to emphasizing idea of prevention and control, strengthening immigration surveillance, improving diagnosis ability, enhancing public health education, and expanding monitoring range.

OBJECTIVETo investigate the pretreatment effects of Rhodiola rosea (R. rosea) extract on cognitive dysfunction, oxidative stress in hippocampus and hippocampal neuron injury in a rat model of Alzheimer's disease (AD).

METHODSMale Sprague-Dawley rats were pretreated with R. rosea extract at doses of 1.5, 3.0, and 6.0 g/kg for 3 weeks, followed by bilateral intracerebroventricular injection with streptozotocin (1.5 mg/kg) on days 1 and 3. Behavioral alterations were monitored after 2 weeks from the lesion using Morris water maze task. Three weeks after the lesion, the rats were sacrificed for measuring the malondialdehyde (MDA), glutathione reductase (GR) and reduced glutathione (GSH) levels in hippocampus and histopathology of hippocampal neurons.

RESULTSThe MDA level was significantly increased while the GR and GSH levels were significantly decreased with striking impairments in spatial learning and memory and severe damage to hippocampal neurons in the model rat induced by intracerebroventricular injection of streptozotocin. These abnormalities were significantly improved by pretreatment with R. rosea extract (3.0 g/kg).

CONCLUSIONR. rosea extract can protect rats against cognitive deficits, neuronal injury and oxidative stress induced by intracerebroventricular injection of streptozotocin, and may be used as a potential agent in treatment of neurodegenerative diseases such as AD.

Animals ; Behavior, Animal ; drug effects ; Biomarkers ; metabolism ; Cell Count ; Cognition Disorders ; chemically induced ; drug therapy ; physiopathology ; Hippocampus ; drug effects ; pathology ; Injections, Intraventricular ; Male ; Neurons ; drug effects ; pathology ; Neuroprotective Agents ; pharmacology ; Oxidative Stress ; drug effects ; Phytotherapy ; Plant Extracts ; pharmacology ; therapeutic use ; Rats ; Rats, Sprague-Dawley ; Rhodiola ; metabolism ; Streptozocin ; administration & dosage ; Swimming ; physiology

OBJECTIVETo exploit the role of bone marrow (BM) and peripheral blood (PB) fluorescence in situ hybridization (FISH) in cytogenetic evaluation of myelodysplastic syndrome (MDS).

METHODSThe metaphase cytogenetics and BM interphase FISH were prospectively compared in 112 cases of de novo MDS. At the same time, comparison of BM and PB FISH was conducted in 56 cases.

RESULTSThe differences between metaphase cytogenetics and BM FISH were observed in 22 (54%) of 41 cases with clonal karyotypic abnormalities, most of differences were caused by the limitation of FISH probe panel which could not target all of the regions with aberrations. Only 6 (27%) of 22 differences were involved in our probe regions, the FISH results did not change their cytogenetic risk categories. BM FISH testing was abnormal in 15 (21%) of 71 cases with normal karyotypes, FISH testing was abnormal in 14/51 (27%) and 1/20 (5%) cases with fewer than 20 normal metaphases or more than 20 normal metaphases. Comparison of FISH results of PB and BM samples showed abnormal PB FISH results in 21 (72%) of 29 cases with abnormal BM FISH results, and in 1 (4%) of 27 cases with normal BM FISH results.

CONCLUSIONBM FISH should be used to MDS cases with fewer than 20 normal metaphases. Although PB FISH testing is limited by a relatively high false negative rate, it is a reasonable choice to cases with failure of BM aspiration.

Adolescent ; Adult ; Aged ; Female ; Humans ; In Situ Hybridization, Fluorescence ; Karyotyping ; Male ; Middle Aged ; Myelodysplastic Syndromes ; blood ; genetics ; Prospective Studies ; Young Adult

OBJECTIVETo analyze significances of different cytogenetic categories for prognostic stratification in patients with primary myelodysplastic syndromes (MDS).

METHODSChromosomal abnormalities of 532 primary MDS patients were categorized according to cytogenetic categories of International Prognostic Scoring System (IPSS), Revised IPSS (IPSS-R), and German-Austrian (G-A). Prognostic impacts of different cytogenetic categories and frequent isolated anomalies were investigated.

RESULTSOf 532 patients, 346(65%) patients had clonal cytogenetic abnormalities, including 200(38%) patients had 1 abnormality, 61(11%) patients had 2 abnormalities, and 85(16%) patients had complex abnormalities. Trisomy 8 was the most frequent karyotype abnormality, occurring in 31% of the patients with clonal cytogenetic abnormalities, other frequent anomalies were -7/del(7q)(13%), del(20q)(12%), del(5q)(9%), -18(5%), -21(5%), i(17q)(5%), -Y(4%), -17(4%), +21(4%), -13/del(13q)(4%), and -22(4%). The proportion of poor karyotypes of IPSS was higher in RAEBI and RAEBII among the World Health Organization classifications than in subgroups with less than 5% blasts. The follow-up data were available for 310 patients with a median follow-up duration of 14.5 months. Median survival was 59 months for patients with normal karyotypes and 26 months for those with abnormal karyotypes. According to IPSS cytogenetic categories, the median survivals of good-risk subgroup, intermediate-risk subgroup and poor-risk subgroup were 59, 43 and 12 months, respectively (P < 0.01). For IPSS-R cytogenetic groups, the median survivals of good-risk subgroup, intermediate-risk(int-risk) subgroup, poor-risk and very poor-risk subgroup were 59, 36, 15, and 10 months, respectively (P < 0.01). According to G-A classification, the median survivals of good-risk subgroup, int-1-risk subgroup, int-2-risk subgroup and poor-risk subgroup were 59, 44, 15, and 11 months, respectively (P < 0.01). In frequent isolated karyotypic abnormalities, +8 had a median survival of 44 months, i(17q) had a median survival of 12 months, and -7/del(7q) had a median survival of 14 months.

CONCLUSIONIn comparison with IPSS and G-A categories, IPSS-R cytogenetic categories are more sophisticated, and can stratify prognosis effectively, but prognostic significances of some karyotypes in IPSS-R still need to be confirmed.

Abnormal Karyotype ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Female ; Humans ; Karyotype ; Male ; Middle Aged ; Myelodysplastic Syndromes ; classification ; diagnosis ; genetics ; Prognosis ; Young Adult

OBJECTIVETo observe the protective effect of Panax notoginseng saponins (PNS) on the level of synaptophysin ptotein in brain in rat model with Alzheimer's disease (AD).

METHODThe AD rat models were established by intra-peritoneal injection of D-galactose combined with excitatory neurotoxin ibotenic acid injection into bilateral nbM. The activity and content of synaptophysin protein in brain were determined by immunohistochemistry analysis.

RESULTPNS could reduce the lesion of level of synaptophysin protein in brain, as compared with those of model group's rats.

CONCLUSIONPNS plays a protective role by reducing down of the level of synaptophysin protein in brain in lesion of AD animal model.

Alzheimer Disease ; chemically induced ; metabolism ; pathology ; Animals ; Basal Nucleus of Meynert ; drug effects ; pathology ; Brain ; metabolism ; pathology ; Galactose ; toxicity ; Ginsenosides ; isolation & purification ; pharmacology ; Ibotenic Acid ; toxicity ; Neuroprotective Agents ; isolation & purification ; pharmacology ; Panax ; chemistry ; Plants, Medicinal ; chemistry ; Rats ; Rats, Wistar ; Synaptophysin ; metabolism

The aim of study is to explore the characteristics of cytogenetics and molecular biology in patients with eosinophilia. Bone marrow samples from 79 cases of eosinophilia (AEoC ≥ 1.5×10(9)/L) were detected for PDGFRA/B and FGFR1 gene rearrangement by fluorescence in situ hybridization and reverse transcription polymerase chain reaction (RT-PCR). Forty-four samples were detected for T cell receptor (TCR) clonal rearrangement by PCR. The results showed that among 76 cases the FIP1L1/PDGFRA (F/P) fusion gene was detected in 19 cases, the CHIC2 deletion was detected in 19 cases, the PDGFRA rearrangement was detected in 4 cases, and no FIP1L1 rearrangement was detected. According to the 2008 WHO classification, diagnosis were revised as myeloid neoplasms with PDGFRA/B rearrangement in 20 (42%) of 48 patients and 5 (83%) of 6 patients with hypereosinophilia syndrome (HES) or chronic eosinophilic leukemia (CEL), respectively. The diagnosis in (17%) of 6 patients with CEL was revised as chronic eosinophilic leukemia, not otherwise as specified (CEL-NOS). Clonal cytogenetic abnormalities were detected in 1 case of CEL-NOS and 3 cases with PDGFRB rearrangement. Karyotypic abnormalities involved in chromosome 4q12 were not detected in all of the 21 cases with PDGFRA rearrangement. The clonal TCR gene rearrangement were detected in 33% (5/15), 40% (6/15), and 36% (5/14) cases with PDGFRA/B rearrangement, HES, or secondary eosinophilia, respectively. There was no statistical difference in incidence rate among 3 subgroups. It is concluded that PDGFRA/B rearrangement can be detected in many cases of HES or CEL. Interphase FISH and PCR testing can enhance the diagnostic rate of myeloid neoplasms with PDGFRA/B rearrangement.
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Female ; Gene Rearrangement ; Humans ; Hypereosinophilic Syndrome ; genetics ; In Situ Hybridization, Fluorescence ; Karyotyping ; Male ; Middle Aged ; Oncogene Proteins, Fusion ; genetics ; Receptor, Fibroblast Growth Factor, Type 1 ; genetics ; Receptor, Platelet-Derived Growth Factor alpha ; genetics ; Receptor, Platelet-Derived Growth Factor beta ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Young Adult ; mRNA Cleavage and Polyadenylation Factors ; genetics

Objective: Analysis of the molecular characteristics of eosinophilia. Methods: Targeting sequence to 24 patients with chronic eosinophilic leukemia (CEL) with rearrangement of PDGFRA, PDGFRB, or FGFR1 and 62 patients with hyper-eosinophilic syndrome (HES). Mutation annotation and analysis of amino acid mutation using authoritative databases to speculate on possible pathogenic mutation. Results: Thirty-seven kinds of clonal variant were detected from 17 patients with CEL, no recurrent mutation site and hot spot region were found. No pathogenic mutation was detected in 19 patients with PDGFRA rearrangement, but pathogenic mutations of ASXL1, RUNX1 and NRAS were detected from 2 patients with FGFR1 rearrangement who progressed to acute myeloid leukemia and 1 patient with PDGFRB rearrangement who progressed to T lymphoblastic lymphoma, respectively. One hundred and two kinds of clonal abnormalities were detected in 49 patients with HES. The main hot spot mutation regions included: CEBPA Exon1, TET2 Exon3, ASXL1 Exon12, IDH1 Y208C, and FGFR3 L164V. CRRLF2 P224L and PDGFRB R370C point mutations were detected separately in 2 patients with HES who treated with imatinib monotherapy and achieved hematologic remission. Conclusion: The pathogenesis of CEL with PDGFRA, PDGFRB or FGFR1 rearrangement is usually single, and the progression of the disease may involve other driver mutation. A variety of genes with hot mutation regions may be involved in the pathogenesis of HES, and some mutation sites are sensitive to tyrosine kinase inhibitors.
Chronic Disease ; Humans ; Hypereosinophilic Syndrome ; Imatinib Mesylate ; Leukemia ; Receptor, Platelet-Derived Growth Factor alpha ; Receptor, Platelet-Derived Growth Factor beta

Objective: To evaluate clinical characteristics and prognosis of primary myelofibrosis (PMF) patients with thrombocytopenia in varied degrees. Methods: Clinical features and survival data of 1 305 Chinese patients with PMF were retrospectively analyzed. The prognostic value of thrombocytopenia in patients with PMF was evaluated. Results: 320 subjects (47%) presented severe thrombocytopenia (PLT<50×10(9)/L), 198 ones (15.2%) mild thrombocytopenia [PLT (50-99)×10(9)/L] and 787 ones (60.3%) without thrombocytopenia (PLT ≥ 100×10(9)/L). The more severe the thrombocytopenia, the higher the proportions of HGB<100 g/L, WBC<4×10(9)/L, circulating blasts ≥ 3%, abnormal karyotype and unfavourable cytogenetics (P<0.001, P<0.001, P=0.004, P<0.001 and P<0.001, respectively) were observed in this cohort of patients. The more severe the thrombocytopenia, the lower the proportion of JAK2V617F positive (P<0.001) was also noticed. Platelet count was positively correlated with splenomegaly, HGB and WBC (P<0.001, correlation coefficients were 0.131, 0.445 and 0.156, respectively). Platelet count was negative correlated with constitutional symptoms and circulating blasts (P=0.009, P=0.045, respectively; correlation coefficients were -0.096 and -0.056, respectively). The median survival of patients with severe thrombocytopenia, mild thrombocytopenia and without thrombocytopenia were 32, 67 and 89 months, respectively (P<0.001). Multivariate analysis identified thrombocytopenia in varied degrees (HR=1.693, 95%CI 1.320-2.173, P<0.001) and Dynamic Internation Prognostic Scoring System(DIPSS) prognostic model (HR=2.051, 95%CI 1.511-2.784, P<0.001) as independent risk factors for survival. Conclusion: PMF patients with severe thrombocytopenia frequently displayed anemia, leucopenia, circulating blasts and short survival, so active treatment measures should be taken especially in these patients.
Humans ; Primary Myelofibrosis ; Prognosis ; Retrospective Studies ; Thrombocytopenia

Objective: To evaluate the efficacy and tolerability of ruxolitinib combined with prednisone, thalidomide and danazol for treatment of in myelofibrosis (MF). Methods: Patients of MF according to the WHO 2016 criteria, received ruxolitinib (RUX) combined with prednisone, thalidomide and danazol (PTD). The response, changes of blood counts and adverse events were evaluated. Results: Six PMF and one post-ET MF patients were enrolled. Four patients presented JAK2V617F mutation, one CALR mutation, one MPL mutation, one triple-negative. Responses per IWG-MRT criteria were clinical improvement in 5 patients, stable disease in 2 ones, spleen response in 6 ones. All of 7 patients were symptomatic responses, four patients achieved at least 50% improvement from baseline on MPN-SAF TSS. Three patients initially treated with RUX alone, all of 3 patients experienced treatment-associated anemia and thrombocytopenia. Then these 3 patients received RUX combined with PTD, both hemoglobin and platelet increased significantly. Four patients initially treated with RUX combined with PTD. Increased levels of hemoglobin and platelet were seen in all of 7 patients received RUX combined with PTD with maximum increased hemoglobin of 30(18-54) g/L and maximum increased platelets of 116(13-369)×10(9)/L, respectively from baseline. The treatment dose of RUX increased due to improved platelet count in 3 patients. The frequent non-hematologic adverse events grade 1-2 were constipation, abdominal distension, crura edema and increased ALT. Conclusions: RUX combined with PTD for treatment of MF may modulate initial hematologic toxicity observed when RUX alone, and may increase response due to improved levels of hemoglobin or platelet.
Danazol ; Drug Combinations ; Humans ; Nitriles ; Pilot Projects ; Prednisone ; Primary Myelofibrosis/drug therapy* ; Pyrazoles/therapeutic use* ; Pyrimidines ; Thalidomide/therapeutic use* ; Treatment Outcome

Objective: To explore the clinical implications and prognostic value of TP53 gene mutation and deletion in patients with myelodysplastic syndromes (MDS) . Methods: 112-gene targeted sequencing and interphase fluorescence in situ hybridization (FISH) were used to detect TP53 mutation and deletion in 584 patients with newly diagnosed primary MDS who were admitted from October 2009 to December 2017. The association of TP53 mutation and deletion with several clinical features and their prognostic significance were analyzed. Results: Alterations in TP53 were found in 42 (7.2%) cases. Of these, 31 (5.3%) cases showed TP53 mutation only, 8 (1.4%) cases in TP53 deletion only, 3 (0.5%) cases harboring both mutation and deletion. A total of 37 mutations were detected in 34 patients, most of them (94.6%) were located in the DNA binding domain (exon5-8) , the remaining 2 were located in exon 10 and splice site respectively. Patients with TP53 alterations harbored significantly more mutations than whom without alterations (z=-2.418, P=0.016) . The median age of patients with TP53 alterations was higher than their counterparts[60 (21-78) years old vs 52 (14-83) years old, z=-2.188, P=0.029]. TP53 alterations correlated with complex karyotype and International prognostic scoring system intermediate-2/high significantly (P<0.001) . Median overall survival of patients with TP53 alterations was shorter than the others[13 (95%CI 7.57-18.43) months vs not reached, χ(2)=12.342, P<0.001], while the significance was lost during complex karyotype adjusted analysis in multivariable model. Conclusion: TP53 mutation was more common than deletion in MDS patients. The majority of mutations were located in the DNA binding domain. TP53 alterations were strongly associated with complex karyotype and always coexisted with other gene mutations. TP53 alteration was no longer an independent prognostic factor when complex karyotype were occurred in MDS.
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Genes, p53 ; Humans ; In Situ Hybridization, Fluorescence ; Middle Aged ; Mutation ; Myelodysplastic Syndromes/genetics* ; Prognosis ; Tumor Suppressor Protein p53 ; Young Adult