Collateral disease theory has been applied to investigate the pathogenesis of chronic dermal ulcer in traditional Chinese medicine. It is suggested that deficiency of vital qi is the pathological basis of chronic dermal ulcer with collaterals stagnation as the major pathological factor, and collaterals impairment by toxin evil is the main pathological change. The important principle in treatment of chronic dermal ulcer is established as strengthening the body resistance, dredging collaterals and removing toxins, and this enriched the theory of wound healing in traditional Chinese medicine, and has practical value.

The clinical thinking modes of "integrative disease and Syndrome" and "integrative macroscopical Syndrome-differentiation and microscopical Syndrome-differentiation" formed in the past half century were merely the primary train of thought and methodology of integrative traditional Chinese and Western medicine. In order to develop them to a higher level, stress should be put on the unity and holism of disordered organism and unity of function, structure and metabolism. It has long been ignored that a parallel and correlated relationship exists between the TCM Syndrome and pathological process of Western medicine, which is a common, set-formed and regular pathophysiological changes with certain development phase, presented in various diseases. Both have common features as that the same pathological process can be seen in different diseases and several pathological progresses can present in one disease, the same Syndrome also can be seen in different diseases and several Syndromes can present in a disease. Moreover, they have the compatible connotation and denotation. The author deduced that pathophysiological basis of main Syndrome is indeed the basic pathological process. Essence of Syndrome is the related pathological processes including abnormal changes in function, metabolism and morphological structure.
Biomedical Research ; methods ; Clinical Medicine ; methods ; Drug Therapy, Combination ; Holistic Health ; Humans ; Medicine, Chinese Traditional ; methods ; Pathology, Clinical ; methods

OBJECTIVE: To explore the effects of Chinese herbs for replenishing qi and resolving stagnation on hypoxia-inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) in granulation tissue of skin ulcers in rats with syndrome of blood stasis and qi deficiency. METHODS: Diabetic rats with back full-thickness skin lesion and syndrome of blood stasis and qi deficiency were divided in to five groups: untreated group, basic fibroblast growth factor (bFGF)-treated group, Yiqi Huayu Recipe (a recipe for replenishing qi and resolving stagnation)-treated group, Yiqi Recipe (a recipe for replenishing qi)-treated group and Huayu Recipe (a recipe for resolving stagnation)-treated group, and another eight normal rats served as normal control group. Immunohistochemical method and image analysis were used to test the expressions of HIF-1alpha and VEGF in granulation tissue of skin ulcers in rats with diabetes. RESULTS: In the untreated group, the expression of HIF-1alpha was significantly increased and the expression of VEGF was significantly decreased as compared with those in the normal control group (P<0.01). The expression of HIF-1alpha was obviously lower (P<0.01) and the expression of VEGF was significantly higher in the four drug treated groups as compared with those in the untreated group. In the Yiqi Huayu Recipe-treated group, the expression of HIF-1alpha was obviously lower than those in the bFGF-treated, Yiqi Recipe-treated and Huayu Recipe-treated groups (P<0.05 or P<0.01), and the expression of VEGF was significantly higher than that in the bFGF-treated group (P<0.01). CONCLUSION: Chinese herbs for replenishing qi and resolving stagnation can promote the wound healing in rats through reducing the expression of HIF-1alpha, accelerating the expression of VEGF in granulation tissue of skin ulcers in rats with diabetes and ameliorating the status of ischemia and hypoxia.

ObjectiveTo compare the efficacy and side effects of ilioinguinal/iliohypogastric nerve blockades and rectal paracetamol after pediatric inguinal hernia repair.MethodsNinety children undergoing half inguinal hernia repair were randomly divided into 3 groups:nerve block group(n=30),paracetamol group(n=30) and control group(n=30).After basal anesthesia,ilioinguinal/iliohypogastric nerve blockades was administed in nerve block group,paracetamol group received rectal paracetamol,control group had not any medication.Every child was oberserved 1,3,6,8 h postoperatively for pain score,overall satisfaction were evaluated by parents,furthermore,evaluation of distress for children such as nausea,vomiting and delayed femoral nerve palsy was made.ResultsPain scores were significantly lower in nerve block group and paracetamol group during the postoperative follow-up 1,3 and 6 h.Overall satisfaction in nerve block group and paracetamol group were significantly higher than control group.The incidence of delayed femoral nerve palsy in nerve block group was higher than paracetamol group(F=4.22P

BACKGROUNDTenidap is a liposoluble non-steroidal anti-inflammatory drug that is easily distributed in the central nervous system and also inhibits the production and activity of cyclooxygenase-2 (COX-2) and cytokines in vitro. This study aimed to evaluate the neuroprotective effect of tenidap in a pilocarpine rat model of temporal lobe epilepsy (TLE).

METHODSTenidap was administered daily at 10 mg/kg for 10 days following pilocarpine-induced status epilepticus (SE) in male Wistar rats after which prolonged generalized seizures resulted in TLE. After tenidap treatment, spontaneous recurrent seizures (SRSs) were recorded by video monitoring (for 7 hours per day for 14 days). The frequency and severity of the SRSs were observed. Histological and immunocytochemical analyses were used to evaluate the neuroprotective effect of tenidap and detect COX-2 expression, which may be associated with neuronal death.

RESULTSThere were 46.88 ± 10.70 survival neurons in tenidap-SE group, while there were 27.60 ± 5.18 survival neurons in saline-SE group at -2.4 mm field in the CA3 area. There were 37.75 ± 8.78 survival neurons in tenidap-SE group, while there were 33.40 ± 8.14 survival neurons in saline-SE group at -2.4 mm field in the CA1 area. Tenidap treatment significantly reduced neuronal damage in the CA3 area (P < 0.05) and slightly reduced damage in the CA1 area. Tenidap markedly inhibited COX-2 expression in the hippocampus, especially in the CA3 area.

CONCLUSIONTenidap conferred neuroprotection to the CA3 area in a pilocarpine-induced rat model of TLE by inhibiting COX-2 expression.

Animals ; Cyclooxygenase 2 ; metabolism ; Epilepsy, Temporal Lobe ; chemically induced ; drug therapy ; metabolism ; Indoles ; therapeutic use ; Male ; Neuroprotective Agents ; therapeutic use ; Pilocarpine ; toxicity ; Rats ; Rats, Wistar

Animals ; Chemical and Drug Induced Liver Injury ; drug therapy ; Liver ; drug effects ; pathology ; Mice ; Silymarin ; pharmacology ; Ursodeoxycholic Acid ; pharmacology

Diagnosis, Differential ; Diagnostic Errors ; Diaphragm ; diagnostic imaging ; physiopathology ; Echinococcosis, Hepatic ; diagnosis ; pathology ; surgery ; Female ; Hernia, Diaphragmatic ; diagnosis ; diagnostic imaging ; Humans ; Liver ; parasitology ; pathology ; surgery ; Tomography, X-Ray Computed

Autophagy, an evolutionarily conserved process by which components of the cell are degraded in lysosomes, may facilitate survival of cancer cells under stress conditions. 8-Azaguanine (8-AG), an inhibitor of purine nucleotide biosynthesis, shows antineoplastic activity in multiple tumor cells. However, chemoresistance has restricted its development as an anticancer agent, and the mechanism of 8-AG resistance is not fully understood. We report here that 8-AG induces a protective autophagy to eliminate its cytotoxicity, and inhibition of autophagy increases cellular sensitivity of cancer cells to 8-AG treatment. Using HepG2 or SMMC-7721 hepatic cancer cell lines, we found that 8-AG inhibited cell viability and induced intrinsic apoptosis, accompanied by the up-regulation of the pro-apoptotic protein BimS, one of Bim (also known as BCL-2-like protein 11, BCL2L11) isoforms. Furthermore, 8-AG treatment enhanced the autophagy flux by promoting the dephosphorylation and activation of Unc-51-like autophagy activating kinase 1 (ULK1) via Akt/mTORC1 (mammalian target of rapamycin complex 1) signaling inhibition. Depletion of autophagy-related gene 7 (ATG7) markedly enhanced the level of BimS, and promoted cell death in response to 8-AG. 8-AG in combination with autophagy inhibitor chloroquine (CQ) or bafilomycin A1 (Baf A1) promoted the 8-AG-induced apoptosis in hepatic cancer cells. Altogether, these findings suggest that autophagy promotes chemoresistance of cancer cells for 8-AG, and blocking autophagy increases cellular sensitivity of cancer cells to 8-AG treatment.

This study was aimed to establish the real-time fluorescent quantitative PCR (RT-qPCR) with erythrocyte Kidd blood group gene for detecting the hematopoietic chimera and to investigate the feasibility of this method. The TaqMan MGB probes and special primers were designed on basis of difference of erythrocyte Kidd blood group alleles, the hematopoietic chimerism was detected by RT-qPCR, the DNA chimerism was simulated by means of dilution of multiple proportions, and the sensitivity analysis was performed. The results showed that the RT-qPCR with erythrocyte Kidd blood group gene could effectively distinguish JK*A and JK*B alleles. There was no significant difference between the theoretic value and the practical measured value by this method (P > 0.05). As 156 donor's cells could be discriminated from 10(4) chimeric cells, this method may effectively detect donor's cells with correlation coefficient 0.998. It is concluded that the established RT-qPCR with erythrocyte Kidd blood group gene shows the feasibility for quantitative detection of hematopoietic chimera, and may be used to quantitatively detect chimera in a certain range.
Chimera ; Erythrocytes ; Humans ; Kidd Blood-Group System ; genetics ; Real-Time Polymerase Chain Reaction

OBJECTIVEWith the objective of discovering novel putative chromosomal regions and special genes involved in the carcinogenesis, progression and metastasis of laryngeal squamous cell cancer (LSCC).

METHODSDNA copy profile of LSCC were obtained and analyzed by comparative genomic hybridization (CGH) and a computerized digital image analysis system. cDNA microarray of LSCC was performed and the profile was analyzed by Hierarchical clustering.

RESULTSCGH analysis showed average-12.9 gains and losses of chromosomes in LSCC. Relatively high frequencies of gains were found at 3q15-21 (14/18), 5p12-13 (11/18), 8q22-24 (6/18), 11q12-13 (8/18), 15q21-23 (7/18) and 18p11 (8/18), while those of losses at 1p13-21 (8/18), 3p21-23 (14/18), 5q21-22 (14/18), 9p12-pter (11/18) and 13q21-31 (8/18). Hierarchical clustering analysis showed that the differentially expressed genes were segregated into three groups. Three genes differentially expressed in process I (normal tissue to cancer) and process II (cancer to lymph node metastasis), and the Cy5/Cy3 ratios of twelve genes were either higher than 5.0 or lower than 0.2 in process I or process II. The fifteen special genes were first reported possibly to be the relationships with LSCC. In particular, 4 genes of them, which were cytochrome C oxidase Va, PPBP, EPHX2 and PON1, were first reported to correlate with tumorigenesis. SH3GL2, which was one of the 15 special genes, was located at one of the special chromosome regions, 9p12-pter.

CONCLUSIONThe important genes and special chromosomal aberrances might provide us a clue for further investigation of carcinogenesis, progression and metastasis in LSCC.

Adult ; Aged ; Carcinoma, Squamous Cell ; genetics ; pathology ; Chromosome Aberrations ; DNA, Neoplasm ; analysis ; Disease Progression ; Female ; Gene Expression ; Humans ; Karyotyping ; Laryngeal Neoplasms ; genetics ; pathology ; Male ; Middle Aged ; Neoplasm Metastasis ; Nucleic Acid Hybridization ; Oligonucleotide Array Sequence Analysis