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Zhengzhou, China

Henan University of Traditional Chinese Medicine is a public university located in Zhengzhou, Henan, China.One of the earliest of its kind in China, Henan University of Traditional Chinese Medicine was established in 1958. It was authorized by the State Academic Council to confer Bachelor’s and Master’s degrees, and to collaborate with other universities or colleges in enrolling doctorate students. It was also approved by the Ministry of Education to enroll international students as well as students from Hong Kong, Macau, and Taiwan.HUTCM offers Bachelor’s degrees in medicine, management, engineering science, and arts with 14 specialties as Chinese medicine, herbology, pharmaceutical engineering, acupuncture and tuina, integrated Chinese-Western medicine, and public management. It also offers Master degrees in 21 specialties, including Chinese internal medicine, Chinese pediatrics, herbal prescriptions, herbology, acupuncture and Tuina are the key programs of Henan Province.The University faculty includes 15 doctoral tutors, 94 professors, 425 associate professors, 714 lecturers on campus, and 16 state-nominated and 10 province-nominated distinguished specialists. HUTCM has presently over 10000 students including over 150 international students. It comprises 20 laboratories, and 3 hospitals besides a central lab, a herbal plantation for quality control, a pharmaceutical factory, and specimen rooms. A number of institutions have been established in this university in the studies of Zhang Zhong-jing’s theories, AIDS, hepatic diseases, gerontology, splenic and gastric diseases, pediatrics, rheumotoid arthritis, and ophthalmology. The University library has a collection of over 500,000 volumes, and over 2,000 varieties of periodicals both from home and abroad. Wikipedia.


Wang J.-H.,Henan University of Traditional Chinese Medicine
Chinese Journal of Integrative Medicine | Year: 2012

Adaptation is an eternal theme of biological evolution. The paper aims at exploring the conception of positive correlation between traditional Chinese medicine (TCM) and human homeostatic evolution based on medical perspective. Discussions mainly involve TCM conforming to natural laws and natural evolution of life, spontaneous harmonization of yin and yang and operating system of human self-healing, modern human immunology and human endogenous immune function in TCM, self-homeostasis of human micro-ecological state and balance mechanism on regulating base in TCM, as well as adaptation-eternal theme of biological evolution and safeguarding adaptability-value of TCM. In perspective of medicine, theory and practice of TCM are in positive correlation with human homeostatic evolution, and what TCM tries to maintain is human intrinsic adaptive capability to disease and nature. Therefore, it is the core value of TCM, which is to be further studied, explored, realized and known to the world. © 2012 The Chinese Journal of Integrated Traditional and Western Medicine Press and Springer-Verlag Berlin Heidelberg. Source


Wang Y.,Henan University of Traditional Chinese Medicine | Wang D.H.,Michigan State University
Endocrinology | Year: 2012

Substance P (SP), a neurokinin-1 receptor (NK-1R) agonist, is mainly produced and stored in primary sensory nerves and, upon its release, participates in cardiovascular and renal functional regulation. This study tests the hypothesis that activation of the NK-1Rs by SP occurs during hypertension induced by deoxycorticosterone (DOCA)-salt treatment, which contributes to renal injury in this model. C57BL/6 mice were subjected to uninephrectomy and DOCA-salt treatment in the presence or absence of administration of selective NK-1 antagonists, L-733,060 (20 mg/kg·d, ip) or RP-67580 (8 mg/kg·d, ip). Five weeks after the treatment, mean arterial pressure determined by the telemetry system increased in DOCA-salt mice but without difference between NK-1R antagonist-treated or NK-1R antagonist-untreated DOCA-salt groups. Plasma SP levels were increased in DOCA-salt compared with control mice (P < 0.05). Renal hypertrophy and increased urinary 8-isoprostane and albumin excretion were observed in DOCA-salt compared with control mice (P < 0.05). Periodic acid-Schiff and Masson's trichrome staining showed more severe glomerulosclerosis and tubulointerstitial injury in the renal cortex in DOCA-salt compared with control mice, respectively (P <0.05). Hydroxyproline assay and F4/80-staining showed that renal collagen levels and interstitial monocyte/macrophage infiltration were greater in DOCA-salt compared with control mice, respectively (P < 0.05). Blockade of the NK-1R with L-733,060 or RP-67580 in DOCA-salt mice suppressed increments in urinary 8-isoprostane and albumin excretion, interstitial monocyte/macrophage infiltration, and glomerulosclerosis and tubulointerstitial injury and fibrosis (P<0.05). Thus, our data show that blockade of the NK-1Rs alleviates renal functional and tissue injury in the absence of alteration in blood pressure in DOCA-salt-hypertensive mice. The results suggest that elevated SP levels during DOCA-salt hypertension play a significant role contributing to renal damage possibly via enhancing oxidative stress and macrophage infiltration of the kidney. Copyright © 2012 by The Endocrine Society. Source


Lu M.,Henan University of Traditional Chinese Medicine
Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine / Zhongguo Zhong xi yi jie he xue hui, Zhongguo Zhong yi yan jiu yuan zhu ban | Year: 2011

To explore the molecular biological mechanism of acupuncture and moxibustion (A&M) in reducing chemotherapy-related toxicity, relieving myelosuppression and increasing peripheral white blood cells (WBC). Two hundred and twenty-four male Kunming mice of clean grade were randomized equally into 4 groups, the blank control group (A), the model group (B), the acupuncture group (C), and the moxibustion group (D). Except those in Group A, mice were duplicated into myelosuppression model with cyclophosphamide (CTX) using the accepted method. After being modeled, mice in Group C and D were treated with acupuncture and moxibustion respectively, once a day for 7 successive days, while those in Group A and B were dealt with the same actions (seizing and fixing) every day but no therapy was given. From day 2 to day 7 of the treatment, 8 mice were taken from every group per day and killed in batches. Their peripheral WBC was counted and bone marrow for detecting Cyclin D1 expression and percentages of bone marrow cells in different cycle stages using immunohistochemistry and flow cytometer respectively. WBC count restored to exceed the baseline in group C and D at day 5 of the treatment, being one day earlier than that in group B. Cyclin D1 expression in the bone marrow raised in Group C and D, and reached the peak at day 4, showing significant difference as compared with that in Group B (P < 0.01). The phase G1 marrow cell percentages in Group C and D was lower than that in Group B at all days of detection, showing statistical significance at day 2-4 (P < 0.05 or P < 0.01); while the percentages of phase S and G2-M cells in the two treated groups was higher than that in group B all the times. While CTX damaged marrow cells, it intervened the cell cycle regularity and reduced the DNA content to cause myelosuppression and leucocytopenia. A&M therapy could improve the Cyclin D1 expression, speed up the cell transition from phase G1 to phase S and increase the synthesis of DNA. At the mean time, taking advantage of the block at phase G2, it can repair the injured DNA, speed up cell mitosis for turning into multiplication, improve the anti-injury and repairing ability of cells to protect bone marrow cells, and relieve the myelosuppression. Source


Wang S.,Henan University of Traditional Chinese Medicine
Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery | Year: 2011

To discuss the effectiveness of antibiotic-impregnated cement temporary spacer for osteomyelitis and nonunion of bone caused by intramedullary fixation. Between June 2002 and May 2006, 12 patients with chronic osteomyelitis and nonunion of bone caused by intramedullary nailing were treated, including 8 males and 4 females with an average age of 40.2 years (range, 26-53 years). The fracture locations included tibia in 7 cases and femur in 5 cases. Infection occurred within 2 weeks after intramedullary fixation in 7 cases and within 3 months in 5 cases. The mean time from infection to admission was 5 months (range, 1-24 months). The results of bacteria culture were positive in 10 cases and negative in 2 cases. White blood cell (WBC) count, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) were higher than normal values. An antibiotic-impregnated cement temporary spacer was inserted after removal of biomembrane and internal fixator, thorough debridement and irrigation. After osteomyelitis was controlled by antibiotic therapy postoperatively, two-stage bone transplantation and internal fixation were performed after 3 to 6 months. All wounds healed by first intention without early complication. All cases were followed up 24 to 48 months (mean, 34 months). WBC count, ESR, and CRP were normal at 3 months postoperatively. The X-ray films showed the fracture healing at 10-14 weeks after operation (mean, 12 weeks). Expect one patient had knee range of motion of 90 degrees, the lower limb function of the others returned to normal. No infection recurred during follow-up. Antibiotic-impregnated cement temporary spacer could control osteomyelitis and nonunion of bone caused by intramedullary nailing, and two-stage bone transplantation and internal fixation after osteomyelitis is an effective and ideal way to treat osteomyelitis and nonunion of bone caused by intramedullary nailing. Source


Wang Y.,Henan University of Traditional Chinese Medicine | Wang D.H.,Michigan State University
Molecular Medicine | Year: 2011

To investigate the effects of the transient receptor potential vanilloid type 1 (TRPV1) channel on renal extracellular matrix (ECM) protein expression including collagen deposition and the transforming growth factor β (TGF-β)/Smad signaling pathway during salt-dependent hypertension, wild-type (WT) and TRPV1-null (TRPV1 -/-) mutant mice were uninephrectomized and given deoxycorticosterone acetate (DOCA)-salt for 4 wks. TRPV1 gene ablation exaggerated DOCA-salt-induced impairment of renal function as evidenced by increased albumin excretion (μg/24 h) compared with WT mice (83.7 ± 7.1 versus 28.3 ± 4.8, P < 0.05), but had no apparent effect on mean arterial pressure (mmHg) as determined by radiotelemetry (141 ± 4 versus 138 ± 3, P > 0.05). Morphological analysis showed that DOCA-salt-induced glomerulosclerosis, tubular injury and macrophage infiltration (cells/mm2) were increased in TRPV1 -/- compared with WT mice (0.74 ± 0.08 versus 0.34 ± 0.04; 3.14 ± 0.26 versus 2.00 ± 0.31; 68 ± 5 versus 40 ± 4, P < 0.05). Immunostaining studies showed that DOCA-salt treatment decreased nephrin but increased collagen type I and IV as well as phosphorylated Smad2/3 staining in kidneys of TRPV1 -/- compared with WT mice. Hydroxyproline assay and Western blot showed that DOCA-salt treatment increased collagen content (μg/mg dry tissue) and fibronectin protein expression (%β-actin arbitrary units) in the kidney of TRPV1 -/- compared with WT mice (26.7 ± 2.7 versus 17.4 ± 1.8; 0.93 ± 0.07 versus 0.65 ± 0.08, P < 0.05). Acceleration of renal ECM protein deposition in DOCA-salt-treated TRPV1 -/- mice was accompanied by increased TGF-β1, as well as phosphorylation of Smad2/3 protein expression (%β-actin arbitrary units) compared with DOCAsalt- treated WT mice (0.61 ± 0.07 versus 0.32 ± 0.05; 0.57 ± 0.07 versus 0.25 ± 0.05; 0.71 ± 0.08 versus 0.40 ± 0.06, P < 0.05). These results show that exaggerated renal functional and structural injuries are accompanied by increased production of ECM protein and activation of the TGF-β/Smad2/3 signaling pathway. These data suggest that activation of TRPV1 attenuates the progression of renal fibrosis possibly via suppression of the TGF-β and its downstream regulatory signaling pathway. © 2011 The Feinstein Institute for Medical Research. Source

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