Ninety normal subjects were determined by the respofnse of the skin to sunlight, and were classified as sun--reactive skin types of Ⅲ, Ⅳ, Ⅴ,most of them were type Ⅳ (80. 11 % ),to the next were types Ⅴ and Ⅲ. The minimal erythema dose (MED) to UVB and UVA,and the immediate pigment darkening reaction(IPD) to UVA radiation were measured for each type. Bivariate correlation analysis showed a positive correlation between the MED UVB and MED- UVA (r= 0. 47d, P＜O. 001 ). The mean IPDUVA was significantly lower than the mean MED--UVA. Both mean MED--UVB and MED--UVA were significantly higher among the subjects in this study in comparison with the English people with skin types Ⅱ and Ⅲ. The validity of sun--reactive skin type in the study on photosensitive skin diseases and phototherapy is discussed.

Objective:To study the anatomic and clinical experience in distally based neuroadipofascial turnover flap incorporating superficial peroneal nerve.Methods:Thirty six (32 preserved and 4 fresh) cadaver lower limbs were used to investigate the blood supply of superficial peroneal nerve and the relationship with the vascularization of its vicinity integument.Distally based neuroadipofascial flap incorporating the nutrifying vessels of superficial peroneal nerve was designed for dorsal foot reconstruction.Results:The proximal part of superficial peroneal nerve was supplied by an accompanying superficial peroneal artery.In the one third part of the lower leg,this artery became an interlacing paraneural vascular plexus and was reinforced by branches from the distal perforators of anterior tibial artery,the supramalleolar perforator of peroneal artery,and the recurrent branches of dorsal pedal artery.Two chain linked longitudinal vascular plexuses (fascial and paraneural) were confirmed in the anterior lower leg integument.In practice,distally based superficial peroneal neuroadipofascial turnover flaps were successfully transferred in 5 cases.The flap measured (10 14) cm?(4 5) cm in size.The pedicle was (3 4) cm in width.The pivot point was located (2 3) cm above the line between medial and lateral malleolus.Conclusion:Distally based superficial peroneal neuroadipofascial turnover flap is a simple and safe procedure with minimal morbidity of the donor site.

Objective To explore the relationships between the expression of PECAM-1 and the degree of ALI in Paraquat induced lung injury model of rabbits. Method Thirty six adult New Zealand rabbits were randomly divided into three groups: 8 mg/kg (Group A), 16 mg/kg (Group B) and 32 mg/kg ( Group C) according to the dose of Paraquat which were infusion into stomach. After poisoned, the animals were monitored for seven days, and then sacrificed. The upper lobe of lung were removed for HE,Masson staining and immunohistochemisty. The ALl score, fibrosis of lung and expression of PECAM-1 were semiquantitative analyzed. Results Each group has 12 animals suffered from poisoning. The survival time of animals in Group C was (6. 47 ± 0. 99 ) days, shorter than (6. 09 + 1.04) days ( P = 0. 031 ) in Group B and (4. 77 + 2. 04) days ( P = 0. 0 07) in Group A. The ALI score were ( 8. 33 ± 1.03) points in Group A, superior to (9. 83 ± 1.17) points ( P = 0. 047 ) in Group B and ( 11.50 + 1.38) points ( P ＜ 0. 01 ) in group C, Group B vs Group C, P=-0.03o The fibrosis degree of lung was (31.09 +2.05)% in Group A,not severe as (34. 37 ±1.62)% (P=0. 002) in Group B and (36. 54 ±0. 44)% (P ＜0. 01 ) in Group C, Group B vs Group C, P = 0. 026. The Pearson correlation analysis showed the expression of PECAM-1 was negative correlated to ALI score (Coe = -0. 732, P =0. 001 ) and fibrosis degree of lung (Coe = -0. 779, P ＜ 0. 001 ) . Conclusions The expressions of PECAM-1 were significantly decreased in New Zealand after Paraquat poisoned, which were dose dependent, correlated to ALI scored and fibrosis degree of lung, so it may play an important role in the development of lung injured induced by Paraquat.

Objective To investigate the p53 gene mutations in Chinese patients with epithelial skin cancers. Methods Biopsies of 22 squamous cell carcinoma(SCC)and 18 basal cell carcinoma(BCC)were analyzed by polymerase chain reaction denaturing gradient gel electrophoresis(PCR-DGGE) and DNA sequencing for alterations in the exons 5～8 of p53 tumor suppressor gene. Results p53 gene mutations were found in 32.5%(13/40)of tumor tissues and 92.3%(12/13) of the mutations occurred at sun exposed areas. 36.4%(8/22)of SCC tissues and 27.8%(5/18) of BCC tissues presented p53 gene mutations. Of the 13 mutations within the exons examined, 76.9%(10/13) were missense mutations and 23.1%(3/13) were nonsense mutations. Twelve of the 13 mutations were of single nucleotide substitutions. Six of the 13 mutations involved dipyrimidine sites, where a C was replaced by a T or CC was replaced by TT(five C→T transitions and one CC→TT transition). Conclusion Ultraviolet(UV) radiation might be related to the pathogenesis of skin cancer. Mutations of p53 gene caused by solar UV might play a significant role in UV tumorigenesis, although other carcinogens might also be involved.

Objective To establish a method of murine local lymph node assay (LLNA) combined with measurement of ear swelling for the identification of photosensitive agents. Methods The female BALB/c mice received test chemicals or vehicle alone on the back skin of both ears and then were exposed to UVA irradiation on three consecutive days. The post-auricular lymph nodes draining the ear tissue were excised 24 h following the last irradiation. Lymph node cell counts and lymphocyte proliferative rates were determined, which indicated lymph node hyperplasia. While ear swelling was also measured, to reveal skin irritating reactions. Some cytokines (IFN-?, IL-2 and IL-4) released by the draining lymph node were also analyzed by ELISA. Results Tetrachlorosalicylanilide, a strong photoallergen, caused lymph node hyperplasia without ear swelling. The mild photoallergen (6-methylcoumarin) showed neither lymph node proliferation nor ear swelling reactions. But 8-methoxypsoralen, a phototoxic substance, induced both lymph node hyperplasia and ear swelling. The level of IL-4 was significantly increased when the mice were previously sensitized with tetrachlorosalicylanilide (P

Objective To investigate the expression of Th1/Th2 cytoki nes in early symptomatic syphilitic lesions and its relationship with the sero-c onversion of RPR test in patients with syphilis. Methods The expression of Th1/Th2 cytokines in lesions from 30 patients with early symptomatic syphilis was i mmunohistochemically detected with ABC method. The serum titers of RPR test in t hese patients were measured in 1, 3, 6, 9 and 12 months after routine benzathine penicillin treatment. Results Among 10 cases of primary syphilis, the express ion of both Th1 and Th2 cytokines in the lesions was found in 9 cases, while onl y Th1 cytokine expression was observed in the remainder case; and the sero-conve rsion of RPR test occurred in all 10 cases during the follow-up period. Among 20 cases of secondary syphilis, Th1/Th2 cytokines expressed in the lesions in 16 c ases, and only Th2 cytokines expressed in 4 cases; and the sero-conversion of RP R test was found in 12 cases during the follow-up period. The expression of Th1 cytokines in early syphilitic lesions was positively correlated with the sero-co nversion of RPR test. The higher the expression of IFN- the more likely the s ero-conversion of RPR test. Conclusion The early activation and persistence of the expression of Th1 cytokines may play an important role in the clearance of pathogens.

Objective To investigate the effects of photochemotherapy on the angiogenic ability of endothelial cells and expression of integrin. Methods In vitro angiogenesis assay ( UVA exposure dose: 0, 2.0, 5.0 J/cm~2) was used to detect the effects of photochemotherapy on the angiogenic ability of endothelial cells. Reverse polymerase chain reaction and flow cytometry were employed to determine the effects of photochemotherapy on the expression of integrin mRNA and protein, respectively. bFGF stimulation group and PMA stimulation group were divided according to the inductors, and subgroups were divided according to the UVA exposure doses of 0, 2. 0 and 5. 0 J/cm~2 in each group. Results Combination of UVA (2.0 and 5.0 J/cm~2) and 8-MOP (100 ng/mL) resulted in a decrease in the angiogenic ability of endothelial cells in vitro and the expression of integrin mRNA and protein. Conclusion Photochemotherapy may inhibit the angiogenic ability of endothelial cells through downregulating the expression of integrin.

Objective To study the effect of neuronal Nogo-66 receptor (NgR1) antagonist,soluble Nogo-66 receptor (sNgR1-Fc),on promoting the endogenous neural precursor cells (NPCs) differentiating into neurons in order to clarify the mechanism.Methods The cortical infarction was induced by photochemistry,named photothrombotic cortical injury (PCI).Twelve Sprague Dawley rats were randomly divided (random number) into three groups:Sham-operated group,PBS group,and sNgR1-Fc group.PBS (PBS group) or sNgR1-Fc (sNgR1-Fc group) was injected into the lateral ventricle of brain with a minipump.BrdU (Bromodeoxyuridine) was injected into the peritoneal cavity 4-6 days after PCI.The subdentate gyrus zone (SGZ) of brain from sacrificed rat was harvested for Immunohistochemistry to observe the ratio of NeuN +/BrdU + cells 35 days after PCI.Proteins including Nestin、Notch1 and Mash1 were detected by Western Blot.Results The cortical infarction in rat was successfully induced by photochemistry.Thirty-five days after PCI,the BrdU + cells number and theratio of NeuN +/BrdU + in the SGZ of the ipsilateral cerebrum hemisphere with PCI were significantly higher in sNgR1-Fc group than those in PBS group (P ＜ 0.05).The levels of Notch1,Mash1 and Neuro D in the sNgR1-Fc group were significantly higher than those in the PBS group (P ＜ 0.05),which were significantly higher than those in the Sham-operated group.Conclusions sNgR1-Fc could promote the endogenous NPCs differentiating into neurons in a cortical infarction model.The mechanisms may be attributed to the Notch/bHLH (proneural basic helix-loop-helix genes) signaling way.

Objective To investigate whether Ulinastatin (UTI) would minimize the systemic inflammatory response,lessen cardiac dysfunction and protect neurons against injury in hippocampus CA1area after restoration of spontaneous circulation (ROSC). Methods Animal models of cardiac arrest were established in 24 New Zealand rabbits,and those animals were randomly (random number) divided into control group and UTI treated group after ROSC.Changes in the levels of plasma inflammatory cytokines TNF-α and IL-6 were assayed before cardiac arrest and 4,8,12 and 16 hours after ROSC.Cardiac function including FS,EF and E/A were observed with ultrasonography before cardiac arrest and 4,8,12 and 16hours after ROSC,and viable and apoptotic neurons in hippocampus CA1 area and infiltrations of MPO positive cells in myocardium,cerebrum,liver,kidney and intestine were counted 72 hours after ROSC.The t-test or Mann-Whitney rank sum test was used to verify the specified theoretical distribution functions of the biomarkers tested by Kolmogorov-Smirnov test,POST HOC test was used for the multiple comparisons,and Pearson correlation analysis was used to investigate the correlation between inflammatory cytokines and cardiac function. Results The levels of TNF-α and IL-6 in UTI group were lower than those in control group as those data got 4,8,12 and 16 hours after ROSC (P ＜0.05).EF and E/A in UTI treated group were higher than those in the control group as those data got 4,8,12 hours after ROSC.FS values obtained 4 h and 8 hours after ROSC were higher in UTI group than those in control group ( P ＜ 0.05 ).The Pearson correlation analysis showed that the levels of TNF-α and IL-6 significantly correlated with EF after ROSC.The number of viable neurons in CA1 area of control group was ( 13.22 ± 0.97) which was lower than that in UTI group ( 16.89 ± 1.45 ) ( P =0.003 ),while the number of apoptotic neurons in hippocampus CA1 area was higher in control group than that in UTI group (15.67 ± 1.37) vs.(13.67 ± 1.03 ) (P =0.019).The numbers of MPO positive cells were significantly lower in liver,kidney and intestine in group UTI than those in control group. Conclusions UTI could inhibit the infiltration of MPO positive cells in liver,kidney and intestine,decreasing the levels of TNF-α and IL-6 in plasma,in turn lessening cardiac dysfunction and protecting neurons from injury in hippocampus CA1 area after ROSC of New Zealand rabbits.

Objective To observe the protective effects of soluble Nogo-66 receptor (NgR1 )antagonist (sNgR1-Fc) on cortical axons after cortical infarction in rats,and to study the phenomenon and molecular mechanism of its protective effects on and regeneration of axons.Methods The cortical infarction was induced by photochemistry,termed photothrombotic cortical injury (PCI).Fifteen Sprague Dawley rats were randomly divided into three groups:Sham-operated group,PBS (phosphate buffered solution) group,and s-NgR1-Fc group.In PBS group,PBS was injected into the lateral ventricle of rats; and in sNgR1-Fc group,sNgR1-Fc was injected instead of PBS. The ipsilateral cortex with lesion was harvested for histomorphometry and transmission electron microscope observation 7 days after PCI. Proteins including GTP-RhoA,p-JNK,p-c-JUN and p-ATF-2 were detected by Western blot,as well as Total-J and Total-RhoA.Results The cortical infarction in rats was successfully induced by photochemistry.Compared with sham-operated group,the pathological changes in PBS groups were more serious,including extensive edema or disappearance of axoplasm of fiber without medulla sheath involved and extensive thickening or layer derangement in axoplasm of fiber with medulla sheath involved.These changes were improved significantly after sNgR1-Fc treatment.The levels of GTP-RhoA,p-JNK1,p-JNK2,p-c-JUN and p-ATF-2 in the PBS group were significantly higher than those in the sham-operation group ( P ＜ 0.05 ),whereas the levels of Total-RhoA,Total-JNKl and Total-JNK2 were not different significantly between these two groups (P ＞0.05 ).The sNgR1-Fc treatment up-regulated the levels of these proteins ( P ＜ 0.05 ).Conclusions There is pathological change in axon induced by cerebral hypoxia-ischemia for a long period after cortical infarction.The mechanisms may be associated with RhoA/ROCK/JNK/c-Jun signal way,which is activated by ischemia injury and related to the inhibition of regeneration in axon.Our study shows that NgR1-Fc may inhibit this pathway significantly,and then promote the regeneration of axon partially.