BACKGROUND: Avascular necrosis of the femoral head occurs in the hip joints at high load-bearing areas, it is a special form of aseptic bone necrosis. Bone marrow-derived mesenchymal stem cells may have an excellent repair effect for the necrosis of femoral head. OBJECTIVE: To understand bone marrow mesenchymal stem cell transplantation for treatment of early avascular necrosis of the femoral head, and to lay a foundation for further study. METHODS: Taking avascular necrosis of femur head, femur head necrosis, osteonecrosis, bone marrow mesenchymal stem cells, mesenchymal stem cells, multipotent stem cells in English as search terms, Pubmed database from January 2000 to April 2009 was retrieved; Taking avascular necrosis and bone marrow mesenchymal stem cells in Chinese as search terms, CNKI database from January 1989 to April 2009 was searched, Literatures were limited to English and Chinese languages. Inclusive criteria: Study of the biological characteristics and functions of bone marrow mesenchymal stem cells, the etiology and pathology of avascular necrosis of femoral head, bone marrow mesenchymal stem cell transplantation for treatment of avascular necrosis; Exclusive criteria: duplication of documents. RESULTS AND CONCLUSION: More than 800 literatures were screened out by computer search, according to inclusive and exclusive criteria, 38 documents of which were involved for analysis. Marrow mesenchymal stem cells can differentiate into chondrocytes, osteocytes and dipocytes under suitable cultural condition. With the development of stem cell engineering, marrow mesenchymal stem cell transplantation becomes an effective method for repairing osteonecrosis. This article describes the cause and the pathology of avascular necrosis of the femoral head, analyzes the theory basis for the treatment of avascular necrosis of the femoral head with marrow mesenchymal stem cell, and verifies its effect through comparing both animal and clinical experiments of this aspect at home and abroad, with the hope of seeking a better treatment.

Objective To achieve systemic and efficient management of the hospital variety of medical equipment,simplify the day -to -day inspection of work. Methods The software part's development used Delphi7.0 and SQL Sever 2000 separately as the onstage development kit and the backstage database; the hardware part,Anti-metal Mifare1 card as the RFID tag,MSR-100 and HDT-3000 as reader were used. Results Test to the system indicates that in the 0～40 mm scope,both of the readers can accurately read and write the tag which adheres to the metal surface,and almost without direction limit. Conclusion Compared with ordinary data bank administration software,this system not only has the basic function such as data's increase,deletion,revision,preservation,backup and restore and so on,but also realizes information exchange between the electronic tag and the database through the serial port and the corresponding submodule; The handle-reader's application especially makes the complicated daily inspection easy and readily achievable,which improves maintenance efficiency,meets the needs of efficient dynamic medical equipment management.

OBJECTIVE:To give some information for developing,using and integrating the available resources of R&D efficiently and accelerating the R&D of new drugs.METHODS:Using scale economic and imitational innovational theory,the current situation of R&D of new drugs at home and abroad were dicussed in terms of resource organization and selection of topic.RESULTS&CONCLUSION:Development of scale economics can benefit the R&D of new drugs in China and imita?tional innovation is a practical way in the present stage.

OBJECTIVE:To provide references for the reformation of private drug wholesale enterprises in Chi?na.METHODS:The private drug wholesale enterprises in China were analyzed in respect to its strength,weakness,opportuni?ties and threats.RESULTS&CONCLUSION:Losing no chances for the reforming of the private drug wholesale enterprises in China is helpful to its development.

Drug Combinations ; Drug Design ; Drugs, Chinese Herbal ; pharmacology ; Drugs, Investigational ; Humans

Aconitum ; poisoning ; Animals ; Disease Models, Animal ; Female ; Hemoperfusion ; methods ; Male ; Plant Poisoning ; therapy ; Rabbits

Animals ; Diazepam ; pharmacology ; Drug Antagonism ; Electroencephalography ; Female ; Male ; Pyrazoles ; poisoning ; toxicity ; Rats ; Rats, Sprague-Dawley

Objective To study the expression and significance of human tissue kallikrein gene 6(KLK6) in cervical cancer tissues.Methods With glyceraldehyde 3-phosphate dehydrogenase (GAPDH)as reference,the expression of KLK6 in 80 cases of cervical cancer tissues (40 cases with metastasis and 40cases without metastasis) and 40 cases of normal cervical tissues was determined by Taqman probe real-time quantitative reverse transcription-polymerase chain reaction,and analyzed the relationship between cervical cancer occurring and KLK6 expression with clinical data and pathological dats.Results The expression of KLK6 in normal cervical tissues[(1.06 ± 0.40) × 10-3] was lower than that in cervical cancer tissues without and with metastasis[(4.41 ± 1.70) × 10-3,(32.22 ± 6.70) × 10-3],and there was significant difference (P＜0.01).The expression of KLK6 in Ⅰ a,Ⅰ b,Ⅱ a stage of cervical cancer tissues with metastasis was (30.42 ± 5.00) × 10-3,(31.64 ± 1.30) × 10-3,(33.02 ± 8.00) × 10-3,and there was no significant difference among them (P ＞ 0.05).The expression of KLK6 in Ⅰ a,Ⅰ b,Ⅱ a stage of cervical cancer tissues without metastasis was (4.12 ± 1.10) × 10-3,(4.35 ± 1.30) × 10-3,(4.82 ± 1.90) × 10-3,and there was no significant difference among them (P＞0.05).There was significant difference in the expreesion of KLK6 in Ⅰ a,Ⅰ b,Ⅱ a stage between cervical cancer tissues with metastasis and cervical cancer tissues without metastasis (P ＜0.01).Conclusion KLK6 can stimulate the cervical cancer cell proliferation,and participate in the progresses of cervical cancer metastasis.

Objective To investigate the impact of hyperthermia on the expression of claudin-1 in focal cerebral ischemia-reperfusion injury in rats and its mechanism in ischemic cerebral injury.Methods A total of 100 male Sprague-Dawley rats were randomly divided into 3 groups:sham operation,normothermia and hyperthermia groups.Both the normothermia and hyperthermia groups were redivided into 3 time points:Ischemia (1 hour) and reperfusion for 3,6,and 24 h.A model of middle cerebral artery occlusion was induced by the intraluminal suture method.At 24 h after reperfusion,brain water content was measured by the wet and dry weight method.The volume of cerebral infarction was assessed by 2,3,5 triphenyl tetrazolium chloride staining.At 3,6,and 24 h after reperfusion,the claudin-1 expression in ischemic brain tissue was measured by Western blot and immunohistochemical staining Results At 24 h after reperfusion,the mean neurological function score in the normothermia group was significantly lower than that in the hyperthermia group (2.3 ± 0.48 vs.3.2 ± 0.63; t =3.576,P =0.002).The brain water content on the operated sides in the sham operation,normothermia and hyperthermia groups was 79.31％ ± 0.60％,81.13％ ± 0.12％,and 84.4％ ± 0.55％,respectively.There were significant differences (F=147.115,P=0.000).Western blot analysis showed that at 3,6,and 24 h after reperfusion,the expression levels of claudin-1 in the normothermia and hyperthermia groups were significantly lower than the sham operation group (all P =0.000),and the expression levels of claudin-1 progressively decreased with the extension of ischemia-reperfusion time (all P ＜ 0.05).At the same time point,the expression level of claudin-1 in the hyperthermia group was significantly lower than that in the normothermia group (all P ＜ 0.01).At 3 and 6 h after reperfusion,the positive expression of claudin-1 among the cerebrovascular endothelial cells was observed in the sham operation,normothermia and hyperthermia groups,while at 24 h after reperfusion,no claudin-1 positive cells were observed.Compared to the sham operation group,at 3 h after reperfusion,the numbers of claudin-1 positive cell and claudin-1 IOD/area (integrated optical density/accumulated positive cell area) in the normothermia and hyperthermia groups begin to decrease,they decreased significantly at 6 h and disappeared at 24 h (P=0.000).At 3 and 6 h after reperfusion,claudin-1 IOD/area in the hyperthermia group was significantly lower than that in the normothermia group (all P ＜ 0.01).Conclusions During cerebral ischemia-reperfusion,hyperthermia may aggravate ischemic brain edema and brain injury by down-regulating the expression of claudin-1 in blood-brain barrier.

Accumulating studies have proved that systemic inflammation is one of the important pathophysiologic mechanisms of heart failure. This article focuses on the sources of inflammation mediators and the causes of inflammation activation in heart failure including hemodynamic changes and oxidative stress, Toll-like receptors, microbial antigens and microorganisms, endotoxin hypothesis and neurohormonal activation. Furthermore, the effects of inflammation mediators such as cytokines and chemokines on heart failure are introduced. All lead to the conclusion that heart failure is a process with complex inflammation.