Objective To compare the effects of transurethral plasmakinetic resection of prostate (TUPKRP) and drug therapy on blood pressure and change of blood pressure rhythm in patients with benign prostatic hyperplasia complicated with hypertension. Methods A total of 103 patients with benign prostatic hyperplasia in the hospital from June 2021 to June 2023 were retrospectively enrolled as study objects. According to different treatment protocols, they were divided into drug therapy group with 47 cases (treated with telmisartan combined with finasteride) and surgical treatment group with 56 cases (treated with telmisartan combined with TUPKRP). Blood pressure levels (24-hour mean diastolic blood pressure, 24-hour mean systolic blood pressure, daytime mean diastolic blood pressure, daytime mean systolic blood pressure, nighttime mean diastolic blood pressure, nighttime mean systolic blood pressure), change of blood pressure rhythm (dipper blood pressure), prostate symptoms, prostate volume, residual urine volume, and sexual function were compared between the two groups before treatment and at 3 and 6 months after treatment. Results The mean blood pressure at different time points in the surgical treatment group was significantly lower than that in the drug therapy group at 3 and 6 months after treatment (P < 0.05). The conversion rates of dipper blood pressure in the surgical treatment group at 3 and 6 months after treatment were 67.86% and 87.50%, which were significantly higher than 40.42% and 68.09% in the drug therapy group (P < 0.05). International Prostate Symptom Score (IPSS), residual urine volume, and prostate volume in the surgical treatment group were significantly lower than those in the drug therapy group at 3 and 6 months after treatment (P < 0.05). There was no significant difference in sexual function between the two groups before treatment and at 3 and 6 months after treatment (P>0.05). Conclusion Telmisartan combined with TUPKRP can reduce blood pressure levels, regulate change of blood pressure rhythm, improve prostate symptoms, reduce prostate volume, and decrease residual urine volume in patients with benign prostatic hyperplasia complicated with hypertension, with minimal impact on sexual function.

The influence of different affinity tags on enzyme characteristics varies. The (S)-carbonyl reductase 2 (SCR2) from Candida parapsilosis can reduce 2-hydroxyacetophenone, which is a valuable prochiral ketones. Different affinity tags, i.e. his-tag, strep-tag and MBP-tag, were attached to the N terminus of SCR2. These tagged SCR2 enzymes, i.e. his6-SCR2, strep-SCR2 and MBP-SCR2, were heterologously expressed in Escherichia coli and purified to study their characteristics towards 2-hydroxyacetophenone reduction. Affinity tags did affect the characteristics of the recombinant SCR2 enzymes. Specifically, affinity tags affect the stability of recombinant SCR2 enzymes: 1) At pH 6.0, the remaining enzyme activities of his6-SCR2 and strep-SCR2 were only 95.2% and 90.0% of the untagged SCR2, while that of MBP-SCR2 was 1.2 times of the untagged SCR2 after incubating for 13 h at 30 °C. 2) The half-life of MBP-SCR2 at 50 °C was 26.6%-48.8% longer than those of strep-SCR2, his6-SCR2 and untagged SCR2. 3) The kcat of MBP-SCR2 was about 1.25-1.45 times of that of small affinity-tagged and untagged SCR2 after storing at -80 °C for 60 d. Structural informatics indicated that the α-helices at the C terminus of MBP-SCR2 contributed to the stability of the N terminus of fusion protein of SCR2. Data from circular dichroism showed that the MBP-tag has some influence on the secondary structure of SCR2, while melting temperature analysis demonstrated that the Tm of the recombinant MBP-SCR2 was about 5 °C higher than that of the untagged SCR2. This study obtained an efficient and stable recombinant SCR2, i.e. the MBP-SCR2. Moreover, this study could serve as a reference for other researchers to evaluate and select appropriate affinity tags for their research.
Alcohol Oxidoreductases ; Escherichia coli/genetics* ; Recombinant Fusion Proteins/genetics*

Objective To evaluate the influencing factors and early recovery quality in elderly patients with gastrointestinal tumor resection by the quality of recovery-40 questionnaire (QoR-40 questionnaire). Methods One hundred and forty- two elderly patients who had underwent gastrointestinal tumor resection from February to June 2017 were selected. The patients were over 65 years old. Their body mass index was (22.98 ± 3.20) kg/m2, and American Society of Anesthesilogists (ASA) wasⅡorⅢgrade. The patients were assessed with QoR-40 questionnaire on the first and second day after operation, and the factors affecting the total score of QoR-40 questionnaire on the first and second day after operation were analyzed. Results Compared with those on the first day after operation, the scores of emotional status, physical comfort, psychological support, physical independence, pain and total score of QoR-40 questionnaire on the second day after operation were significantly higher: 42 (39, 43) scores vs. 40 (38, 42) scores, 53 (52, 54) scores vs. 52 (50, 53) scores, 35 (35, 35) scores vs. 35 (34, 35) scores, 15 (13, 15) scores vs. 14 (12, 15) scores, 34 (33, 35) scores vs. 33 (32, 34) scores and 178 (173, 182) scores vs. 174 (169, 177) scores, and there were statistical differences (P<0.01). On the first day after operation, the total score of the QoR-40 questionnaire was related with the type of operation (P<0.05), and it was not related with age, sex and anesthesia (P>0.05);on the second day after operation, the total score of QoR-40 questionnaire was related with age and operation type (P<0.05), and it was not related with sex and anesthesia (P > 0.05). Conclusions The early postoperative period score of QoR-40 questionnaire in patients with colorectal tumor resection and age less than 70 years old is higher, and the recovery quality after operation is relatively good, suggesting that the operation type and age may be an important factor affecting the early recovery quality of the elderly patients with gastrointestinal tumor resection.

OBJECTIVE: To systematically evaluate the efficacy difference between warming acupuncture and other acupuncture methods in the treatment of primary obesity. METHODS: A computer-based retrieval was conducted at PubMed, EMBASE, CENTRAL, CINAHL, Alt HealthWatch, CNKI, CBM, WANFANG database and VIP database. Retrieval time was from the establishment date of database to October 4, 2017. Randomized controlled trial (RCT) of warming acupuncture comparing with other acupuncture methods for the treatment of primary obesity were included. The relative risk () and weighted mean difference ( ) were used as combined effects for categorical variables and continuous variables, respectively. RESULTS: Totally 13 RCTs were included involving 878 patients. The Meta-analysis indicated compared with other acupuncture methods, warming acupuncture could more reduce weight (: -1.49 kg, 95% : -2.53 to -0.45, =0.005), improve the total effective rate (=1.16, 95% : 1.09 to 1.24, <0.000 01), reduce BMI (: -1.24 kg/m, 95% : -2.34 to -0.14, =0.03), reduce waist circumference (: -1.65 cm, 95% : -2.53 to -0.76, =0.02) and reduce hip circumference (: -2.86 cm, 95% : -4.37 to -1.35, =0.000 2), but had no significant influence on total cholesterol (: -0.05 mmol/L, 95% :-0.98 to 0.88, =0.91). CONCLUSION The warming acupuncture has better efficacy on primary obesity than other acupuncture methods, but less effects on lipid indicators.
Acupuncture Therapy ; Databases, Factual ; Humans ; Lipids ; Obesity ; therapy ; Randomized Controlled Trials as Topic

Arginine deiminase (ADI) was first high-efficient expressed in Corynebacterium crenatum SYPA 5-5. The ADI was purified by Ni-NTA affinity chromatography and SDS-PAGE analysis showed the molecular weight (MW) was 46.8 kDa. The optimal temperature and pH of ADI were 37 ℃ and 6.5 respectively. The Michaelis constant was 12.18 mmol/L and the maximum velocity was 0.36 μmol/(min·mL). Under optimal conditions, 300 g/L of arginine was transformed and the productivity reach 8 g/(L·h). The recombinant strain was cultivated in a 5-L fermentor and used for whole-cell transformation of 300 g/L arginine, under repeated-batch bioconversion, the cumulative production reached 1 900 g/L.

Objective To evaluate clinical efficacy and safety of loratadine combined with desloratadine in the treatment of chronic spontaneous urticaria(CSU)in children. Methods A total of 177 children with CSU were enrolled into this study, and randomly and equally divided into 3 groups:combination group treated with an age?based dose of desloratadine tablet every morning and a weight?based dose of loratadine tablet before sleep every night for consecutive 28 days, loratadine group treated with a half tablet of placebo(starch tablet)every morning and oral loratadine tablet before sleep every night for consecutive 28 days, and desloratadine group treated with a half tablet of placebo (starch tablet) every morning and oral desloratadine tablet before sleep every night for 28 consecutive days. Possible adverse reactions were observed and recorded after the start of treatment, and therapeutic effects were evaluated at the end of treatment. Results A total of 166 patients completed the trial, including 55 in the combination group, 56 in the loratadine group and 55 in the desloratadine group. After 28?day treatment, the total response rate was significantly higher in the combination group(90.9%, 50/55)than in the loratadine group (71.4%[40/56],χ2=6.865, P<0.05)and desloratadine group(74.5%[41/55],χ2=5.153, P<0.05). No significant difference in the incidence of adverse reactions was observed among the combination group (10.9%[6/55]), loratadine group (8.9%[5/56]) and desloratadine group (9.1%[5/55], P > 0.05). Conclusion Combination of loratadine and desloratadine was superior to loratadine or desloratadine alone in the treatment of childhood CSU, and there was no significant difference in the incidence of adverse reactions among the 3 treatment groups.

Non-coding RNAs ( ncRNA ), including ribosomal RNA( rRNA), transfer RNA( tRNA), MicroRNA ( miRNA), long noncoding RNA(lncRNA) and small nucleolar RNA(snoR-NA), are a class of RNA that have multiple functions and are not translated to proteins. MicroRNA and lncRNA are involved in the injury, remodeling and aging of blood vessels, and it is necessary to understand the regulatory roles of MicroRNA and lncRNA in these processes. It is reported that MicroRNA and lncRNA are not only participated in the regulation of oxidative response, inflammation, cell proliferation and migration, and phenotype transition, they are also involved in the regulation of gene expression by conducting different mechanisms, including transcriptional regulation, post-transcriptional modification and chromatin remodeling. These aspects of regulation by MicroRNA and lncRNA are related to cardiovascular diseases, such as ath-erosclerosis, hypertension, myocardial infarction, stroke, pul-monary hypertension and diabetes, and thus provide a new way for genetic diagnosis and therapy of cardiovascular diseases.

OBJECTIVETo investigate the molecular?mechanisms by which triptolide induces apoptosis of human acute T lymphocytic leukemia Jurkat cells.

METHODSMTT assay was employed to detect the proliferation inhibition of Jurkat cells by triptolide, and the IC50 was calculated by OriginPro8. Flow cytometry was used to analyze apoptosis of Jurkat cells. Np9 mRNA levels were detected by RT-PCR and analyzed quantitatively by Kodak 1D 3.6 software. Correlation between the inhibition of Np9 transcription and the cell apoptosis was analyzed by SPSS 19.0.Western blotting was employed to determine Np9 downstream signaling molecules c-myc, β-catenin, ERK, AKT and Notch1 protein level in Jurkat cells after exposure to different concentrations of triptolide for 48 h.

RESULTSTriptolide treatment resulted in dose-dependent inhibition of Jurkat cells proliferation and its IC50 was 12.7 nmol/L. Triptolide induced apoptosis of Jurkat cells in dose- dependent manner. Furthermore, triptolide inhibited Np9 mRNA transcription level in Jurakt cells in a dose-dependent manner. There was a correlation between the triptolide-mediated the apoptosis and the inhibition of Np9 transcription of Jurkat cells (R(2)=0.907). Western blotting results displayed that triptolide inhibited transcription levels of Np9 mRNA with a concomitant decrease of its downstream signaling molecules c-myc, β-catenin, ERK, AKT and Notch1 at protein levels.

CONCLUSIONInhibition of HERV-K Np9 mRNA and its downstream signaling molecules c-myc, β-catenin, ERK, Akt and Notch1 protein might be one of important molecular?mechanisms by which triptolide induces apoptosis of human acute T lymphocytic leukemia Jurkat cells.

Apoptosis ; drug effects ; Diterpenes ; pharmacology ; Endogenous Retroviruses ; genetics ; Epoxy Compounds ; pharmacology ; Flow Cytometry ; Gene Products, env ; genetics ; Humans ; Jurkat Cells ; drug effects ; Phenanthrenes ; pharmacology ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma ; pathology ; Transcription, Genetic

Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder characterized by a chromosome translocation that generates the Bcr-Abl oncogene encoding a constitutive kinase activity. Despite remarkable success in controlling CML at chronic phase by Bcr-Abl tyrosine kinase inhibitors (TKIs), a significant proportion of CML patients treated with TKIs develop drug resistance due to the inability of TKIs to kill leukemia stem cells (LSCs) that are responsible for initiation, drug resistance, and relapse of CML. Therefore, there is an urgent need for more potent and safer therapies against leukemia stem cells for curing CML. A number of LSC-associated targets and corresponding signaling pathways, including CaMKII-γ, a critical molecular switch for co-activating multiple LSC-associated signaling pathways, have been identified over the past decades and various small inhibitors targeting LSC are also under development. Increasing evidence shows that leukemia stem cells are the root of CML and targeting LSC may offer a curable treatment option for CML patients. This review summarizes the molecular biology of LSC and its-associated targets, and the potential clinical application in chronic myeloid leukemia.
Animals ; Chemokines ; metabolism ; Epigenesis, Genetic ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; genetics ; metabolism ; pathology ; Neoplastic Stem Cells ; metabolism ; pathology ; Transcription Factors ; metabolism ; Tumor Microenvironment

Objective To investigate the molecular mechanisms by which triptolide induces apoptosis of human acute T lymphocytic leukemia Jurkat cells. Methods MTT assay was employed to detect the proliferation inhibition of Jurkat cells by triptolide, and the IC50 was calculated by OriginPro8. Flow cytometry was used to analyze apoptosis of Jurkat cells. Np9 mRNA levels were detected by RT-PCR and analyzed quantitatively by Kodak 1D 3.6 software. Correlation between the inhibition of Np9 transcription and the cell apoptosis was analyzed by SPSS 19.0.Western blotting was employed to determine Np9 downstream signaling molecules c-myc,β-catenin, ERK, AKT and Notch1 protein level in Jurkat cells after exposure to different concentrations of triptolide for 48h. Results Triptolide treatment resulted in dose-dependent inhibition of Jurkat cells proliferation and its IC50 was 12.7nmol/L. Triptolide induced apoptosis of Jurkat cells in dose-dependent manner. Furthermore, triptolide inhibited Np9 mRNA transcription level in Jurakt cells in a dose-dependent manner. There was a correlation between the triptolide-mediated the apoptosis and the inhibition of Np9 transcription of Jurkat cells (R2=0.907). Western blotting results displayed that triptolide inhibited transcription levels of Np9 mRNA with a concomitant decrease of its downstream signaling molecules c-myc,β-catenin, ERK, AKT and Notch1 at protein levels. Conclusion Inhibition of HERV-K Np9 mRNA and its downstream signaling molecules c-myc, β-catenin, ERK, Akt and Notch1 protein might be one of important molecular mechanisms by which triptolide induces apoptosis of human acute T lymphocytic leukemia Jurkat cells.