Review of clinical studies of Polygonum multiflorum Thunb. and its isolated bioactive compounds

Photograph used for a newspaper owned by the Oklahoma Publishing Company. Caption: "(photo looking up a building's side that has an outwards build where the window are located and a fence or something similar at the front of the camera)

The Contributive Role of IGFBP-3 and Mitochondria in Synoviocyte-Induced Osteoarthritis through Hypoxia/Reoxygenation Injury: A Pathogenesis-Focused Literature Review

Osteoarthritis (OA), one of the most common joint disorders, is characterized by chronic progressive cartilage degradation, osteophyte formation, and synovial inflammation. OA lesions are not only located in articular cartilage but also in the entire synovial joint. Nevertheless, most of the early studies done mostly focused on the important role of chondrocyte apoptosis and cartilage degeneration in the pathogenesis and progress of OA. The increased expression of hypoxia-inducible factors (HIF-1α and HIF-2α) is known to be the cellular and biochemical signal that mediates the response of chondrocytes to hypoxia. The role of the synovium in OA pathogenesis had been poorly evaluated. Being sensitive to hypoxia/reoxygeneration (H/R) injury, fibroblast-like synoviocytes (FLS) play an essential role in cartilage degradation during the course of this pathology. Insulin-like growth factor binding protein 3 (IGFBP-3) acts as the main carrier of insulin-like growth factor I (IGF-I) in the circulation and remains the most abundant among the six IGFBPs. Synovial fluids of OA patients have markedly increased levels of IGFBP-3. We aim to discuss the interconnected behavior of IGFBP-3 and synoviocytes during the course of osteoarthritis pathogenesis, especially under the influence of hypoxia-inducible factors. In this review, we present information related to the essential role that is played by IGFBP-3 and mitochondria in synoviocyte-induced osteoarthritis through H/R injury. Little research has been done in this area. However, strong evidences show that the level of IGFBP-3 in synovial fluid significantly increased in OA, inhibiting the binding of IGF-1 to IGFR 1 (IGF receptor-1) and therefore the inhibition of cell proliferation. To the best of our knowledge, this is the first paper providing a comprehensive explanatory contribution of IGFBP-3 and mitochondria in synovial cell-induced osteoarthritis through hypoxia/reoxygenation mechanism

Assessment and evaluation efficacy of a clinical pharmacist-led inpatient warfarin knowledge education program and follow-up at a Chinese tertiary referral teaching hospital

Background: Oral anticoagulation therapy with warfarin is used to prevent and to treat venous and arterial thrombosis and embolism. Its narrow therapeutic index should be monitored carefully in order to reach the desired outcomes. Objective: This study aims to evaluate the clinical pharmacist-led in-patient warfarin′s knowledge education program and to assess a follow-up efficacy in a Chinese tertiary referral teaching hospital. Design and Setting: A cross-sectional and observational study was conducted at the Affiliated Hospital of Medical College of Nanjing University, a 1460-bed tertiary referral teaching hospital in Nanjing. Materials and Methods: One-on-one interview questionnaire was conducted among 47 Chinese patients who had undergone prosthetic valve replacement. Before the patient education program′s implemented, at discharge time and 3 months, 6-9 months and 12 months after surgery were considered as time points. A previously validated 17-item questionnaire was used to measure the patient′s knowledge level of warfarin and to assess and evaluate a follow-up efficacy of this patient education program run by a clinical pharmacist. Knowledge scores were compared using the Student′s t-test or one-way analysis of variance. Main Outcome Measure: Patients′ knowledge on the warfarin education program and warfarin knowledge score, drug therapy problems or bleeding complication events associated to warfarin therapy and evaluation of clinical pharmacist′s service provided. Results: Patients mean age was 47.68 ΁ 9.70 years (range 23-67). The higher education strata had significantly higher warfarin knowledge scores (P < 0.05). In terms of hospital stay post-surgery, compared with other groups, patients with an average of 11-14 days, were found significantly and statically higher knowledgeable in warfarin (P < 0.05). The clinical pharmacist′ service was found very satisfying f(80.85%). Conclusion: Chinese patients on warfarin therapy should benefit from periodic educational efforts reinforcing key medication safety information. Patient education is not a once-off procedure. A complete patient education program run by a clinical pharmacist in a Cardio-thoracic ward can considerably improve and enhance to reduce the hospital stays and significantly enlighten the role of the patient education in adherence to therapy

Rhein Elicits In Vitro Cytotoxicity in Primary Human Liver HL-7702 Cells by Inducing Apoptosis through Mitochondria-Mediated Pathway

Objective. To study rhein-induced apoptosis signaling pathway and to investigate its molecular mechanisms in primary human hepatic cells. Results. Cell viability of HL-7702 cells treated with rhein showed significant decrease in dose-dependent manner. Following rhein treatment (25 μM, 50 μM, and 100 μM) for 12 h, the detection of apoptotic cells was significantly analyzed by flow cytometry and nuclear morphological changes by Hoechst 33258, respectively. Fatty degeneration studies showed upregulation level of the relevant hepatic markers (P < 0.01). Caspase activities expressed significant upregulation of caspase-3, caspase-9, and caspase-8. Moreover, apoptotic cells by rhein were significantly inhibited by Z-LEHD-FMK and Z-DEVD-FMK, caspase-9 inhibitor, and caspase-3 inhibitor, respectively. Overproduction of reactive oxygen species, lipid peroxidation, and loss of mitochondrial membrane potential were detected by fluorometry. Additionally, NAC, a ROS scavenger, significantly attenuated rhein-induced oxidative damage in HL-7702 cells. Furthermore, real-time qPCR results showed significant upregulation of p53, PUMA, Apaf-1, and Casp-9 and Casp-3 mRNA, with no significant changes of Fas and Cytochrome-c. Immunoblotting revealed significant Cytochrome-c release from mitochondria into cytosol and no change in Fas expression. Conclusion. Taken together, these observations suggested that rhein could induce apoptosis in HL-7702 cells via mitochondria-mediated signal pathway with involvement of oxidative stress mechanism

Advances in Etiopathological Role and Control of HPV in Cervical Cancer Oncogenesis

The human papillomavirus (HPV) is a well-known oncovirus whose causal link in the occurrence and development of several cancers, such as cervical cancer (CC), has been well established. Indeed, numerous researches depicted the etiological role of HPV in CC pathogenesis in such a way as to develop efficient strategies, including early diagnoses and HPV vaccination, to mitigate HPV infection and CC occurrence. Despite the effectiveness of these strategies in preventing HPV infection, its persistence, and the progression to precancerous lesions and cancers, extensive work that could give a better understanding of other unknown factors favoring oncogenesis is much more needed. In this last decade, scarce or few but crucial and strategic studies have been carried out to improve and deepen our understanding of the etiopathological role of HPV in the progression towards the development of CC. In this review, we highlighted the recent findings on the pathological role of HPV in CC occurrence and the advances in novel adopted strategies to reduce HPV infection and prevent CC occurrence more effectively