39 results match your criteria: "Inner Mongolian Medical University[Affiliation]"

Nano-lanthanum hydroxide, a novel phosphate binder, for treating hyperphosphatemia: A preclinical study.

Biomed Pharmacother

March 2019

Department of Pharmacology, College of Pharmacy, Inner Mongolian Medical University, Jinshan Street, Hohhot 010110, Inner Mongolia Autonomous Region, China. Electronic address:

This study is to determine the pharmacological effects of nano-lanthanum hydroxide (nano-LH) in the treatment of hyperphosphatemia, in comparison with other phosphate binders. Rat models of chronic renal failure and hyperphosphatemia were induced by adenine, which were treated with nano-LH (0.15, 0.

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To clarify distribution and drug resistance characteristics of anaerobes isolated from clinical infectious samples, and to provide experimental data for guiding on treatment of infections caused by anaerobes. The anaerobes, isolated from 1 057 different clinical specimens from inpatients admitted to the Affiliated Hospital of Inner Mongolia Medical University from March 2016 to November 2017, were identified by VITEK-2 anaerobes and corynebacterium (ANC) card and bacteroides fragilis isolates were further verified by 16S-rRNA sequencing. Meanwhile, broth dilution method was employed to detect the drug sensititities of and PCR method was used to detect the carbapenem resistance gene cfiA.

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Huntington's disease (HD) is caused by a cytosine-adenine-guanine (CAG) trinucleotide repeat expansion in the huntingtin (HTT) gene encoding an elongated polyglutamine tract within the N-terminal of the huntingtin protein (Htt) and leads to Htt misfolding, aberrant protein aggregation, and progressive appearance of disease symptoms. Chronic activation of endoplasmic reticulum (ER) stress by mutant Htt (mHtt) results in cellular dysfunction and ultimately cell death. Protein disulfide isomerase (PDI) is a chaperone protein located in the ER.

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Chloroquine inhibits autophagy and deteriorates the mitochondrial dysfunction and apoptosis in hypoxic rat neurons.

Life Sci

June 2018

Southern Medical University, Guangzhou, Guangdong Province, PR China; Departmengt of Pediatrics, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangdong Neuroscience Institute, Guangzhou, Guangdong Province, PR China. Electronic address:

Aims: Mitochondrial dysfunction (MD) and apoptosis in the neurons are associated with neonatal hypoxic-ischemic (HI) encephalopathy (HIE). The present study was to explore the influence of autophagy on the induction of MD and apoptosis in the neurons in a neonatal HIE rats and in hypoxia-treated neurons in vitro.

Materials And Methods: Ten-day-old HI rat pups were sacrificed for brain pathological examination and immunohistochemical analysis.

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Huntington's disease (HD) is an autosomal dominant inherited neurodegenerative disorder, and no cure is available currently. Treatment of HD is likely to be most beneficial in the early, possibly pre-manifestation stage. The challenge is to determine the best time for intervention and evaluate putative efficacy in the absence of clinical symptoms.

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2,4 DNP improves motor function, preserves medium spiny neuronal identity, and reduces oxidative stress in a mouse model of Huntington's disease.

Exp Neurol

July 2017

Division of Neurobiology, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, United States; Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States; Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, United States. Electronic address:

Huntington's disease (HD) is a neurodegenerative disorder caused by a CAG repeat expansion in the first exon of the gene huntingtin. There is no treatment to prevent or delay the disease course of HD currently. Oxidative stress and mitochondrial dysfunction have emerged as key determinants of the disease progression in HD.

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The Antiapoptosis Effect of Glycyrrhizate on HepG2 Cells Induced by Hydrogen Peroxide.

Oxid Med Cell Longev

March 2017

Department of Pharmacology, Pharmacy School, Inner Mongolian Medical University, Jinshan Developing Zone, Hohhot, Inner Mongolia 010110, China.

This study demonstrated that glycyrrhizate (GAS) could protect HEPG2 cells against damage and apoptosis induced by HO (1600 M, 4 h). Cell viability assay revealed that GAS was noncytotoxity at concentration 125 g/mL, and GAS (5 g/mL, 25 g/mL, and 125 g/mL) protected HepG2 cells against HO-induced cytotoxicity. HO induced the HepG2 cells apoptosis, obvious morphologic changes were observed after Hochest 33258 staining, and more apoptotic cells were counted in flow cytometry assay compared to that of the natural group.

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Polygalasaponin XXXII, a triterpenoid saponin from Polygalae Radix, attenuates scopolamine-induced cognitive impairments in mice.

Acta Pharmacol Sin

August 2016

State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica & Neuroscience Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.

Aim: Recent studies show that the extract of a Chinese herb Polygalae Radix exerts cognition-enhancing actions in rats and humans. The aim of this study was to characterize the pharmacological profiles of active compounds extracted from Polygalae Radix.

Methods: Two fractions P3 and P6 and two compounds PTM-15 and polygalasaponin XXXII (PGS32) were prepared.

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Gallbladder agenesis and atrial septal defect: A case report.

Exp Ther Med

May 2016

Department of General Surgery, The Affiliated Hospital of Inner Mongolian Medical University, Hohhot, Inner Mongolia Autonomous Region 010059, P.R. China.

Congenital absence of gallbladder and atrial septal defect (ASD) are clinically rare congenital organ malformations, and the simultaneous occurrence of the two is even more rare. The present study reported a case of gallbladder agenesis combined with congenital ASD. A 38-year-old male patient presented with a 3-year history of recurring upper right abdominal pain.

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[Influence of Mouse Spleen Microenviroment on T-ALL Progression].

Zhongguo Shi Yan Xue Ye Xue Za Zhi

February 2016

Affiliated Hospital of Inner Mongolia Medical University, Hohehot 010050, Inner Mogolian Autonomous Region, China. E-mail:

Article Synopsis
  • The study aimed to understand how the spleen affects the status of T-cell acute lymphoblastic leukemia (T-ALL) in mice by monitoring leukemia cell development in various organs post-transplantation.
  • It was found that the spleen underwent significant changes during T-ALL progression, with a notable increase in T-ALL cells, and its weight fluctuated more than other organs like the liver.
  • Splenectomy, the surgical removal of the spleen, delayed the progression of T-ALL, indicating that the spleen plays a supportive role in the disease's advancement and serves as a key environment for leukemia cells.
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Objective: To explore the molecular epidemiological features and in vitro susceptibility profile of Corynebacterium striatum strains isolated from different sites of inpatients, and further provide new data and idea for clinicians to better get knowledge of the clinical significance of Corynebacterium striatum.

Methods: Fourty-five strains of Corynebacterium striatum isolated from different sites of inpatients from November, 2013 to March, 2014 in Affiliated hospital of Inner Mongolian medical university, and microdilution method was employed to do in vitro antibiotics susceptibility test. Saline-cotton swab method was used to sample the surrounding environmental surfaces for Corynebacterium striatum carrying patients, and suspected colonies were further identified and in vitro drug susceptibility test were performed.

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Notch1-induced T cell leukemia can be potentiated by microenvironmental cues in the spleen.

J Hematol Oncol

November 2014

State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, 300020, China.

Background: Leukemia is a systemic malignancy originated from hematopoietic cells. The extracellular environment has great impacts on the survival, proliferation and dissemination of leukemia cells. The spleen is an important organ for extramedullary hematopoiesis and a common infiltration site in lymphoid malignancies.

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The chemokine-like factor 1 induces asthmatic pathological change by activating nuclear factor-κB signaling pathway.

Int Immunopharmacol

May 2014

State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Department of Pharmacology, Institute of Materia Medica, Chinese Academy of Medical Sciences, Peking Union Medical College, 1 Xiannongtan Street, Xicheng District, Beijing 100050, China. Electronic address:

CKLF1, which exhibits chemotactic activities on a wide spectrum of leukocytes, is up-regulated during the progress of asthma. It plays a vital role in the pathogenesis of pulmonary disease. Here, we report that CKLF1 has the capability to activate the NF-κB signaling pathway leading to the pathological change in the lung.

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Objective: To explore the anti-tumor effects of resveratrol (Res) upon human skin squamous cell carcinoma A431 xenograft in nude mice and elucidate the regulatory mechanisms of survivin and caspase-3.

Methods: The model of human skin squamous cell carcinoma (A431) xenograft in nude mice was established. And the animals were randomly divided into saline-negative control, cyclophosphamide (CTX) positive control, Res high-, medium- and low-dosage and blank control groups (n = 10 each).

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