Through his long-term acupuncture-moxibustion teaching and academic research, professor LI Ding from Shanghai University of TCM had conducted a profound research on the theory of the eight extra meridians, named Governor Vessel, Conception Vessel, Thoroughfare Vessel, Belt Vessel, Link Vessels and Heel Vessels, as well as their relationship with the regular meridians. He rectified the miss-understanding on the courses of Governor Vessel and Conception Vessel determined by the ancient medical masters, and had a further analysis on some different views, such as the running course of Governor Vessel and the flowing direction of meridian qi in Governor Vessel and Conception Vessel. He proposed that the nutrient qi flew up to down in Governor Vessel and down to up in Conception Vessel. His research and discovery much perfected the theory of the eight extra meridians and provided a significant instruction for the research on the eight extra meridians in the later generations.
Acupuncture ; education ; history ; China ; History, 20th Century ; History, 21st Century ; History, Ancient ; Humans ; Male ; Meridians ; Teaching

DOU Han-qing's academic thought of acupuncture and moxibustion are analyzed, which include "eight confluence points", sensation of qi arrival, 14 manipulations for promotion of qi sensation, point selection, needling technique and observation of the psychological condition of patients. DOU's inheritance and development of Huangdi Neijing (Internal Classic) and Nanjing (Classics on Medical Problems) as well as his influences on the later schools are approved to have great value and significance on the enhancement of clinical effect and development of acupuncture and moxibustion sciences.
Acupuncture ; education ; history ; Acupuncture Therapy ; history ; China ; History, Ancient ; Humans ; Moxibustion ; history

BACKGROUNDGalectin-3 is the most recently identified advanced glycosylation end products (AGEs) binding protein. This study aimed to investigate the effects of AGEs and rosiglitazone on the expression and secretion of galectin-3 in cultured human renal mesangial cells (HRMCs).

METHODSHRMCs were incubated with different concentrations of AGE-bovine serum albumin (BSA) (0, 50, 100, 200, and 400 mg/L) for different time (0, 24, 36, 48, and 72 hours), and exposed to AGE-BSA in the presence of different concentrations of rosiglitazone (1, 10, and 100 micromol/L). The mRNA and protein expression of galectin-3 in HRMCs were analyzed by reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. The culture medium of HRMCs was collected and concentrated, and the content of galectin-3 in the medium was detected by Western blotting.

RESULTSBoth RT-PCR and Western blotting revealed that AGE-BSA up-regulated the expression of galectin-3 in HRMCs in a concentration- (P < 0.05) and time-dependent (P < 0.05) manner compared with the control. Compared with the control, AGE-BSA elevated the content of galectin-3 in the culture medium of HRMCs time- and concentration-dependently (P < 0.05, respectively). Both protein and mRNA expression of galectin-3, and its content in the medium of HRMCs exposed to different concentrations of rosiglitazone in the presence of AGE-BSA were increased compared with those of cells exposed to AGE-BSA alone (P < 0.05). Rosiglitazone increased the expression and secretion of galectin-3 in a dose-dependent manner (P < 0.05).

CONCLUSIONSAGEs up-regulates the expression and secretion of galectin-3 in HRMCs. Rosiglitazone further enhances the upregulation of galectin-3 in HRMCs induced by AGEs, which suggests that rosiglitazone may play a role of reno-protection via up-regulation of galectin-3.

Blotting, Western ; Cell Line ; Galectin 3 ; genetics ; secretion ; Glycation End Products, Advanced ; pharmacology ; Humans ; Hypoglycemic Agents ; pharmacology ; Mesangial Cells ; drug effects ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Serum Albumin, Bovine ; pharmacology ; Thiazolidinediones ; pharmacology

Objective To explore the effects of acupuncture on pruritic behaviors, expression of 5-HT neurons in medulla oblongata and 5-HTR2B on mice with chloroquine-induced pruritus; To discuss the mechanism of action of acupuncture in chloroquine-induced pruritus. Methods A non-histamine-dependent pruritus model was prepared by subcutaneous injection of chloroquine into the back of the neck. Forty C57B/6J mice were randomly divided into model-acupuncture group, model-non-acupuncture group, normal saline group and blank control group, with 10 mice in each group. After modeling, acupuncture was given in Xuehai, Quchi and Hegu on both sides. The plug and twist way was used to stimulate, once a day, three times. Model-non-acupuncture group received no acupuncture. Normal saline group received the neck injection of saline in the back. Blank control group received no treatment. Behavioral changes were observed, and immunofluorescence technique and Western blot were used to test the expression of 5-HT neurons and 5-HTR2B in medulla oblongata neurons. Results The number of scratches in model-acupuncture group and model-non-acupuncture group was obviously more than normal saline group and blank control group (P<0.05). The number of scratches in model-acupuncture group was lower than that of model-non-acupuncture group (P<0.05). The expression of 5-HT in medulla oblongata neurons was unclear in both normal saline group and blank control group. The expression of 5-HT neurons in medulla oblongata significantly increased in model group, which decreased after acupuncture. The expression of 5-HTR2B of model group was significant higher than normal saline group and blank control group (P<0.01). Compared with model-non-acupuncture group, the expression of 5-HTR2B in model-acupuncture group significant decreased (P<0.01). Conclusion Acupuncture can significantly inhibitscratching behaviors in mice induced by chloroquine, and the mechanism may be realized by decreasing the expression of 5-HT neurons and 5-HTR2B in medulla oblongata neurons.

OBJECTIVETo investigate the clinical, pathological and immunohistochemical features of vulvar intraepithelial neoplasia (VIN).

METHODSAccording to the 2004 modified terminology of International Society for the Study of Vulvovaginal Diseases (ISSVD), the cases were diagnosed as VIN from patients who had performed vulvar biopsy in Beijing Wuzhou Women's Hospital from February 2009 to December 2011, which were reclassified as usual VIN and differentiated VIN. The clinical and pathological studies were conducted respectively. MaxVision immunohistochemical staining was used to detect the expression of Ki-67, p16 and p53 proteins.

RESULTSThere were 20 cases of VIN in 237 patients, and the incidence of VIN was 8.4% in all of contemporary vulvar biopsy. In 17 cases of usual VIN, mean age was 29.6 years, the lesion typically presented with atypical cells involving almost all layers of the epithelium, which was equivalent to the high-grade squamous intraepithelial neoplasia of cervix. Immunohistochemistry for Ki-67 and p16 was strongly positive in usual VIN. High risk human papillomavirus (HPV) detection was also positive. The incidence of differentiated VIN was less than usual VIN, and there were only 3 cases in this study. In differentiated VIN, patients aged over 50 years, with mean of 53.7 years, and the lesion most commonly presented with lichen sclerosis background. There were epithelial thickening and extending, and parakeratosis, and atypia was strictly confined to the basal and parabasal layers of the epithelium where the cells enlarged with abundant eosinophilic cytoplasm, presented with prominent nucleoli, increased cellularity and abnormal keratinization. In differentiated VIN, p53 was strongly positive, Ki-67 and p16 immunohistochemical expression was confined to the basal layer only.

CONCLUSIONSVIN is a precursor of invasive squamous cell carcinoma of the vulva. The modified terminology of ISSVD classifies VIN as high-grade lesions. Definitive pathological diagnosis of VIN plays an important role in its timely treatment and the prevention of vulvar carcinoma.

Adult ; Carcinoma in Situ ; metabolism ; pathology ; virology ; Cyclin-Dependent Kinase Inhibitor p16 ; metabolism ; Female ; Humans ; Immunohistochemistry ; Ki-67 Antigen ; metabolism ; Middle Aged ; Papillomavirus Infections ; pathology ; Tumor Suppressor Protein p53 ; metabolism ; Vulvar Neoplasms ; metabolism ; pathology ; virology ; Young Adult

PURPOSE: Although the interferon α (IFNα) signaling and the paired-like homeodomain transcription factor 2 (PITX2) have both been implicated in the progression of breast cancer (BCa), it remains obscure whether these two pathways act in a coordinated manner. We therefore aimed to elucidate the expression and function of PITX2 during the pathogenesis of endocrine resistance in BCa. MATERIALS AND METHODS: PITX2 expression was assessed in BCa tissues using quantitative reverse transcription polymerase chain reaction (RT-qPCR) and immunohistochemistry and in experimentally induced letrozole-resistant BCa cells using RT-qPCR and immunoblotting. Effects of PITX2 deregulation on BCa progression was determined by assessing MTT, apoptosis and xenograft model. Finally, using multiple assays, the transcriptional regulation of interferon-inducible transmembrane protein 1 (IFITM1) by PITX2 was studied at both molecular and functional levels. RESULTS: PITX2 expression was induced in letrozole-resistant BCa tissues and cells, and PITX2 induction by IFNα signaling powerfully protected BCa cells against letrozole insult and potentiated letrozole-resistance. Mechanistically, PITX2 enhanced IFNα-induced AKT activation by transactivating the transcription of IFITM1, thus rendering BCa cells unresponsive to letrozoleelicited cell death. Additionally, ablation of IFITM1 expression using siRNA substantially abolished IFNα-elicited AKT phosphorylation, even in the presence of PITX2 overexpression, thus sensitizing BCa cells to letrozole treatment. CONCLUSION: These results demonstrate that constitutive upregulation of PITX2/IFITM1 cascade is an intrinsic adaptive mechanism during the pathogenesis of letrozole-resistance, and modulation of PITX2/IFITM1 level using different genetic and pharmacological means would thus have a novel therapeutic potential against letrozole resistance in BCa.
Apoptosis ; Breast Neoplasms ; Breast ; Cell Death ; Heterografts ; Immunoblotting ; Immunohistochemistry ; Interferons ; Phosphorylation ; Polymerase Chain Reaction ; Reverse Transcription ; RNA, Small Interfering ; Transcription Factors ; Transcriptional Activation ; Up-Regulation

BackgroundThe previous study showed that mycophenolic acid (MPA) synergizing with lipopolysaccharide (LPS) promoted interleukin (IL)-1β release, but the mechanism is unclear. This study aimed to investigate the mechanism of MPA synergizing with LPS to induce IL-1β release.

MethodsUndiluted human blood cells, THP-1 human myeloid leukemia mononuclear cells (THP-1) cells, or monocytes were stimulated with LPS and treated with or without MPA, and the supernatant IL-1β was detected by enzyme-linked immunosorbent assay. The mRNA levels of IL-1β were detected by real-time quantitative polymerase chain reaction. The intracellular protein levels of nuclear factor kappa B (NF-κB) phospho-p65 (p-p65), precursor interleukin-1β (pro-IL-1β), NOD-like receptor pyrin domain containing-3 (NLRP3), and cysteine aspartic acid-specific protease-1 (caspase-1) p20 in THP-1 cell were measured by Western blot.

ResultsThe MPA alone failed to induce IL-1β, whereas MPA synergized with LPS to increase IL-1β in a dose-dependent manner (685.00 ± 20.00 pg/ml in LPS + 5 μmol/L MPA group, P = 0.035; 742.00 ± 31.58 pg/ml in LPS + 25 μmol/L MPA group, P = 0.017; 1000.00 ± 65.59 pg/ml in LPS + 75 μmol/L MPA group, P = 0.024; versus 408.00 ± 35.50 pg/ml in LPS group). MPA alone has no effect on the IL-1β mRNA expression, LPS induced the expression of IL-1β mRNA 2761 fold, and LPS + MPA increased the IL-1β expression 3018 fold, which had the same effect with LPS group (P = 0.834). MPA did not affect the intracellular NF-κB p-p65 and pro-IL-1β protein levels but activated NLRP3 inflammasome. Ac-YVAD-cmk blocked the activation of caspase-1 and subsequently attenuated IL-1β secretion (181.00 ± 45.24 pg/ml in LPS + MPA + YVAD group vs. 588.00 ± 41.99 pg/ml in LPS + MPA group, P = 0.014).

ConclusionsTaken together, MPA synergized with LPS to induce IL-1β release via the activation of caspase-1, rather than the enhanced production of pro-IL-1β. These findings suggested that patients immunosuppressed with mycophenolate mofetil may have overly activated caspase-1 during infection, which might contribute to a more sensitive host defense response to invading germs.

Animals ; Caspase 1 ; metabolism ; Cells, Cultured ; Humans ; Inflammasomes ; Interleukin-1beta ; metabolism ; Lipopolysaccharides ; pharmacology ; Mice ; Mice, Inbred NOD ; Mycophenolic Acid ; pharmacology ; NLR Family, Pyrin Domain-Containing 3 Protein

The hippocampus plays a crucial role in learning and memory, and its progressive deterioration with age is functionally linked to a variety of human neurodegenerative diseases. Yet a systematic profiling of the aging effects on various hippocampal cell types in primates is still missing. Here, we reported a variety of new aging-associated phenotypic changes of the primate hippocampus. These include, in particular, increased DNA damage and heterochromatin erosion with time, alongside loss of proteostasis and elevated inflammation. To understand their cellular and molecular causes, we established the first single-nucleus transcriptomic atlas of primate hippocampal aging. Among the 12 identified cell types, neural transiently amplifying progenitor cell (TAPC) and microglia were most affected by aging. In-depth dissection of gene-expression dynamics revealed impaired TAPC division and compromised neuronal function along the neurogenesis trajectory; additionally elevated pro-inflammatory responses in the aged microglia and oligodendrocyte, as well as dysregulated coagulation pathways in the aged endothelial cells may contribute to a hostile microenvironment for neurogenesis. This rich resource for understanding primate hippocampal aging may provide potential diagnostic biomarkers and therapeutic interventions against age-related neurodegenerative diseases.