[Summary] Pruritus is one kind of skin disease that has itching symptom with no primary skin lesions , may develop excoriation , crust and pigmentation secondary . Pruritus is a common skin complication affecting on patients with diabetes ,which is also one of the clues of early diagnosis .This article focus on the etiology ,pathogenesis ,clinical manifestation ,prevention and treatment of diabetes patients complicated with skin pruritus .

BACKGROUND: Traditional dialysis membranes are mostly synthesized by organic polymer materials. Although these materials can meet the needs of treatment, the pore size range is large and the microtubules are not uniform, which can cause protein clogging on the dialysis membrane. Therefore, it is difficult to achieve the expected therapeutic effect.OBJECTIVE: To study the hemocompatibility of titanium dioxide nanotube bio-dialysis membrane.METHODS: High-strength titanium dioxide nanotube films were prepared by anodic oxidation method, the bottom of the nanotubes was etched by HF gas, and the LLC-PK1 and ECV304 cells were seeded onto the prepared titanium dioxide nanotube array membranes to construct two kinds of titanium dioxide nanotube bio-dialysis membranes. Hemolysis test,dynamic clotting time test and platelet adhesion test were used to determine the hemocompatibility of the prepared titanium dioxide nanotube bio-dialysis membrane.RESULTS AND CONCLUSION: In the hemolysis test, the hemolysis rates of the titanium dioxide nanotube array membranes carrying LLC-PK1 and ECV304 cells were lower than that of the polyurethane material (0.30％, 0.34％,0.56％; P < 0.05). In the dynamic clotting test (20, 40, 70 minutes), the dynamic clotting time of the titanium dioxide nanotube array membranes carrying LLC-PK1 and ECV304 cells were significantly longer compared with the polyurethane material (P < 0.05). In the platelet adhesion test, the platelet adhesion rate showed no significant difference between the polyurethane material and the titanium dioxide nanotube array membranes carrying LLC-PK1 and ECV304 cells (P > 0.05). These findings indicate that the titanium dioxide nanotube bio-dialysis membrane possesses good hemocompatibility.

Objective To investigate the role of Staphylococcus aureus enterotoxin B (SEB) in non-IgE mediated activation of mast cells (MCs) by in vitro co-culture of laboratory of allergic disease 2 (LAD2) cells and SEB.Methods The LAD2 cells were incubated with SEB at different concentrations of 0.01,0.1,1,10 and 100 μg/ml,A23187 positive control and negative control separately for 30 minutes.Then,effects of SEB on the morphology of MCs were observed by using a light microscope,and culture supernatants of the above incubation systems were collected.The concentration of tryptase released from MCs was analyzed by enzymatic activity assay,and the level of histamine was detected by enzyme-linked immunosorbent assay (ELISA).Results After 30-minute co-culture of LAD2 cells and SEB,MCs showed larger size,obscure boundaries,increased number of protuberances on the cell surface and decreased refractivity,with a radial burr fin-like appearance.After 30-minute co-culture of LAD2 cells and SEB at different concentrations of 0.01,0.1,1,10 and 100 μg/ml,the concentrations of tryptase in the culture supematants were 4.116 ± 0.651,5.344 ± 0.874,3.806 ± 0.459,1.309 ± 0.247,0.310 ± 0.199 ng/ml respectively.Additionally,the tryptase levels were significantly higher in the 0.01-,0.1-,1-μg/ml SEB groups than in the negative control group(1.538 ± 0.490,all P ＜ 0.05),and gradually decreased along with the increase of SEB concentrations.The histamine levels in the 0.01-,0.1-,1-,10-and 100-μg/ml SEB groups were 242.409 ± 63.915,522.491 ± 73.466,550.926 ± 84.466,334.397 ± 33.640,226.527 ± 5.678 ng/ml respectively.In the 0.01-,0.1-,1-μg/ml SEB groups,the levels of histamine released from MCs were gradually increased along with the increase of SEB concentrations,and were significantly higher than those in the negative control group (146.436 ± 3.100,all P ＜ 0.05).However,with the continued increase of SEB concentrations,the histamine levels gradually decreased.Conclusion SEB can directly activate MCs by a non-IgE mediated mechanism,followed by morphologic changes of MCs and release of tryptase and histamine.

OBJECTIVE:To observe the effect of atorvastatin combined with methylprednisolone on the liver function of ne-phrotic syndrome patients. METHODS:The data of 93 patients with primary nephritic syndrome were retrospectively analyzed and divided into atorvastatin group,methylprednisolone group and combination group by different medication. Atorvastatin group was orally given atorvastatin 20 mg at bedtime,once a day+aspirin;methylprednisolone group was orally given methylprednisolone 0.8 mg/kg in the early morning,once a day+aspirin;combination group was given atorvastatin+methylprednisolone+aspirin(the same usage and dosage with the above-mentioned groups). The course was 4 weeks. The clinic data was observed,including ALT,AST, GGT,TB and DB before and after treatment,the incidence of patients with drug-induced liver disease and prognosis of patients with drug-induced liver disease. RESULTS:After treatment,the ALT,AST and GGT in atorvastatin group and combination group were significantly higher than before,with significant difference(P<0.05);compared with other parameters and all indexes in methylprednisolone group before and after treatment,there were no significant differences(P>0.05). There was no significant dif-ference in the elevated rate of ALT among groups(P>0.05);the incidence of drug-induced liver disease in combination group was significantly higher than atorvastatin group and methylprednisolone group,with significant difference(P<0.05). ALT in combina-tion group was significantly decreased and returned to pretreatment levels after atorvastatin withdrawal and 2 weeks of hepatoprotec-tants treatment for 7 patients with drug-induced liver disease. CONCLUSIONS:Atorvastatin combined with methylprednisolone has high risk on liver function in the treatment of nephrotic syndrome. Pretreatment levels can be recovered by both drug withdrawal and symptomatic treatment.

Objective To study the inclusion mechanism of 14-deoxyandrographolide and ?-cyclodextrin in inclusion ratio,molecular interaction between host and guest,inclusion part and stability of inclusion compound.Methods The formation of inclusion compound was confirmed by dfferential thermal analysis(DTA);The equilibrium constants of inclusion compound were determined and the thermodynamic constants were calculated by UV;Inclusion parts were confirmed by IR and 1H-NMR.Results Ka=1 292.631 L/mol;?G=-16.854 8;?H=-25.532;?S=-0.029 12.It was clearly that all five lactone ring and decalin ring of 14-deoxyandrographolide in indusion compound changed in IR and 1H-NMR.Conclusion Inclusion host-guest ratio is 1∶1,Van der Waals forces play a major role in the process.Inclusion site is decalin ring and five lactone ring.The inclusion compound is more stable under normal temperature.

BACKGROUND:In the earliest stages of embryonic development and organ formation, fibroblast growth factor family members function as mediating the growth, differentiation, survival, and morphology of progenitor cels. Fibroblast growth factor mediates metabolic function, tissue repair and regeneration in mature tissues by reactivation of signal pathways.
OBJECTIVE:To summarize and explore the role of the fibroblast growth factor signaling pathway in tissues and organs.
METHODS:A computer-based online search was conducted in CNKI and PubMed databases by using the key words of “fibroblast growth factor, signaling pathway” from 2010 to 2016 and 2000 to 2016, respectively to screen the relevant literatures. The language was limited to both Chinese and English. Research progress in the fibroblast growth factor signaling pathway was summarized.
RESULTS AND CONCLUSION:A total of 47 literatures were included. Mammalian fibroblast growth factor family is composed of 18 secreted signal proteins which interact with 4 tyrosine kinase signal fibroblast growth factor receptors. Interaction of fibroblast growth factor ligand with the receptor is regulated by a protein or cofactor binding proteoglycans and extracelular proteins. Activation of fibroblast growth factor receptor mediates interaction with cytoplasmic adapter protein, RAS-MAPK, and PI3K-AKT, phospholipase Cγand STAT signaling pathway by phosphorylation on a specific tyrosine residue. Four structuraly related intracelular non-signaling fibroblast growth factors regulate the voltage-gated sodium ion channels by their interactions. Fibroblast growth factors exist in almost al tissues and organs, and developmental defects and abnormal activity of this pathway (destruction of organogenesis) is associated with damage response to injury, metabolic disorders and cancer.

Objective:To study the masseter motor evoked potential(MEP)in patients with sleep bruxism(SB)and in healthy con-trols.Methods:30 subjects with SB and 30 healthy controls were included.MEPs were obtained by transcranial magnetic stimulation (TMS).Tests were done during daytime when the subjects were awake.The data were statistically analysed.Results:In the patients AMT was 55(52,55)%,latency of c-MEP (6.7 ±1.3)ms,the amplitude of c-MEP 0.19(0.15,0.29)mV,latency of r-MEP (2.3 ±0.4)ms,the central conduction time(CCT)4.4(3.3,5.2)ms.In the control subjects AMT was 52(52,55)%,latency of c-MEP (6.4 ±0.7)ms,the amplitude of c-MEP 0.23(0.17,0.28)mV,latency of r-MEP (2.4 ±0.4)ms,CCT 4.0 (3.4,4.4) ms.No significant difference was found between the 2 groups in the measurements evoked by TMS.Conclusion:The MEP after TMS in patients with SB is similar to that of healthy subjects,indicating that the excitability of the cortical motor system is not changed in bruxism subjects,at least when evaluated by TMS.

Objective To investigate the effects of ursolic acid (UA) on cisplatin (CDDP)-induced expres_sion of transient receptor potential vanilloid 1 (TRPV1) in mouse cochlea .Methods Sixty BALB/c mice were ran_domly divided into 4 groups (15 mice in each group) and received introperitoneal injection once daily for 5 days:Control group (normol saline) ,UA group (80 mg/kg/day) ,CDDP group (4 .5 mg/kg/day) ,and CDPP (4 .5 mg/kg/day) plus UA group (80 mg/kg/day) .The expression of TRPV1 in mouse cochlea was determined by immuno_histochemistry ,microscope image analysis and western blot ,and auditory thresholds were evaluated by auditory brainstem response (ABR) measurement .ResuIts The expression of cochlea TRPV1 and ABR threshold shift was significantly increased in the mice treated with CDDP (P< 0 .05) ,as compared with control mice .These effects were prevented by UA treatment (all P<0 .05) .Furthermore ,a linear relationship analysis revealed that the ex_pression of cochlea TRPV1 was significantly correlated with ABR threshold shift(|r|>0 .7 , P<0 .05) .ConcIusion UA effectively attenuated CDDP -induced ototoxicity and improved auditory function through inhibition of TR_PV1 .

Objective:To establish a method for the determination of content and related substances of troxipite tablets by HPLC. Methods:A Waters Symmetry-C18 (150 mm × 4. 6 mm,5 μm) column was used. The mobile phase was methanol -0. 4% phosphoric acid solution (50∶50). The flow rate was 1. 0 ml·min-1. The detection wavelength was 260nm. The column temperature was 35℃and the injection volume was 20 μl. Results:The linear range of troxipite was 3-75 μg·ml-1(r=0.999 7). The average recovery was 99. 7%,RSD=0. 95%(n=9). Conclusion:The method is simple, accurate and specific, and can be used in the quality control of troxipite tablets.

Objective:To investigate the effects of survivin inhibitor YM155{1-(2-methoxyethyl)-2-methyl-4,9-dioxo-3-(pyrazin-2-ylmethyl)-4,9-dihydro-1H-naphtho[2,3-d] imidazolium bromide} on cell viability,apoptosis and Cysteinyl aspartate specific proteinase-3,Cysteinyl aspartate specific proteinase-8,Cysteinyl aspartate specific proteinase-9 of the thyroid carcinoma cell line B-CPAP in order to discuss mitochondrial mechanisms of apoptosis.Methods: B-CPAP cells were cultured in vitro and treated with YM155 at various concentrations(0,0.5,1,2,4,8 nmol/L)for 24,48 and 72h.The cell viability of B-CPAP cells were measured by CCK-8 assay.B-CPAP cells were randomly divided into 4 groups:B-CPAP cells were treated with YM155 at various concentrations(0,1,2 nmol/L)and 5 μmol/L Cisplatin(the positive control group)for 24 h.The effects of YM155 on B-CPAP cells apoptosis were evaluated by TUNEL and flow cytometry Annexin V-FITC/PI method.The expression level of Survivin and Caspase-3,Caspase-8 ,Caspase-9 were detected by Western blot analysis.Results: Compared with the 0 nmol/L group,YM155 significantly inhibited the cell viability of B-CPAP cells and induced their apoptosis (P<0.05 or P<0.01).Compared with the 0 nmol/L group,YM155 significantly reduced the expression level of Survivin and upregulated Caspase-3,Caspase-8 ,Caspase-9(P<0.05 or P<0.01).Conclusion: YM155 can inhibit the cell viability of B-CPAP cells and induce apoptosis,its possible mechanisms maybe related to upregulated expression level of Caspase-3,Caspase-8 and Caspase-9.