The objective of this study was to examine the inpatient bed (IB) allocation equity and utilization in Chinese city community health service centers (CHSCs). The data were derived from the Baseline Survey of National City Community Health Service System Building Project, which was conducted in 1917 CHSCs in 28 cities in 2007. The IB allocation was analyzed in terms of IB allocation quantity and distribution equity, and the IB utilization was analyzed by the IB utilization rate and average length of stay of the CHSC inpatients. The results showed that 49.3% of the CHSCs were equipped with IB; averagely, there were 45 IBs per CHSC, 0.94 IBs per 1000 people, and 0.38 nurses and 0.57 doctors per IB; the IB Gini coefficient was 0.32; the IB utilization rate was 40.06%; and the average length of stay of inpatients was 12.24 days. The conclusions were that IB allocation among the population was equitable, but the number of nurse per IB was not up to the national standard; and the CHSC IB utilization was low as a whole, thus inpatient service was not the main health service for Chinese CHSCs.

To investigate the effect of autoimmune regulator (AIRE) on phagocytic clearance of apoptotic cells, a recombinant expression vector containing full-length human AIRE cDNA was transfected into 16HBE cells. After incubation with transfected 16HBE cells, engulfment of apoptotic HL-60 cells induced by camptothecin was detected by myeloperoxidase (MPO) staining. The change in the expression of Rac 1 in transfected 16HBE cells was determined by RT-PCR and Western blotting. The results showed that the phagocytosis percentage of the experimental group, the mock transfection group and the negative control group (non-apoptotic cells) was (25.50±3.67)%, (6.25±1.58)% and (1.0±0.67)%, respectively. Moreover, the expressions of Rac 1 mRNA and protein were up-regulated in AIRE-transfected 16HBE cells, suggesting that AIRE may function as a regulator in the phagocytic clearance of apoptotic cells by promoting the expression of Rac 1.

This study examined the effects of a recombinant adenovirus Ad-PTEN-EGFP on the proliferation of A549 cells, a human lung carcinoma cell line, in vitro and on the growth of the implanted tumors in the nude mice in vivo, explored the underlying mechanisms and evaluated the in vitro transfection efficiency of Ad-PTEN-EGFP into A549 cells. The expression of Ad-PTEN-EGFP in the A549 cells was determined. The proliferation and the apoptosis rates of the A549 cells with Ad-PTEN-EGFP transfection or not was detected by MTT and flow cytometry. Ad-PTEN-EGFP at different doses was injected intratumorally to the tumor-bearing mice induced by the A549 cells. Tumor sizes were measured on an alternate day. After all the mice were sacrificed, the implanted tumors were removed for routine histological examination, weight test, HE staining and immunohistochemical staining. The expressions of Bax, P16 and P53 in the tumor tissues and those of caspase-3, CD34 and VEGF in the mouse sera were detected. Tumor cell apoptosis was measured by TUNEL method. The results showed that the vitality of the A549 cells after transfection with Ad-PTEN-EGFP declined. The expression of green fluorescent protein was observed under fluorescent microscope. The transfection rate was in excess of 50%. The mRNA and protein expression of PTEN in the transfected cells was confirmed. The proliferation rate of the transfected cells was significantly decreased when compared with that of the non-transfected cells (P<0.05). The number of the apoptosis cells was increased in the transfected cells (P<0.05). The models of implanted tumors were successfully established by injection of the A549 cells in the flank of Balb/c nude mice. Administration of Ad-PTEN-EGFP to the tumor-bearing nude mice resulted in a suppression of tumor growth. There were statistically significant differences in the tumor weight and tumor volume between the Ad-PTEN-EGFP-treated group and the control groups (P<0.05). In contrast to those in the control groups, tumor tissues in the Ad-PTEN-EGFP-treated group were shown to have typical extensive vacuolar degeneration and massive hemorrhagic necrosis. Apoptotic bodies were also observed in the tumor cells. The expressions of Bax, caspase-3 and P16 were increased (P<0.05) while those of CD34, VEGF and P53 decreased (P<0.05) in the Ad-PTEN-EGFP-treated group. It is concluded that Ad-PTEN-EGFP could induce the apoptosis of the A549 cells and inhibit their proliferation. And it could also substantially suppress the tumor growth in the tumor-bearing nude mice and induce apoptosis of the tumor cells as well. These findings carry significant implications for adenovirus vector-based PTEN gene therapies for lung cancers.

The effects of electric currents applied during absolute refractory period (ARP) on the cardiac function of rabbits with heart failure due to myocardial infarction (MI), and the safety of this method were investigated. Thirty rabbits were randomly assigned equally to 3 groups: sham-operated group, LV-anterior wall cardiac contractility modulation (LV-CCM) group, and septum-CCM (S-CCM) group. A thoracotomy was performed on all the rabbits. Electric pulses were delivered during the ARP on the anterior wall of left ventricle in CCM group and in the septum in S-CCM group, respectively. The left ventricular systolic pressure (LVSP) and maximum positive left ventricular pressure change (+dp/dt_max), heart rates, ventricular tachycardia, ventricular fibrillation were observed. It was found that, as compared with the baseline, LVSP, and +dp/dtmax were significantly increased, on average, by 15.2% and 19.5% in LV-CCM group (P<0.05), and by 8.5% and 10.8% in S-CCM group (P<0.05). LVEDP was significantly decreased and -dp/dt_max increased both in LV-CCM group and S-CCM group (P<0.05). CCM had no effect on heart rate and induced no arrhythmia in short time. It is concluded that electric currents delivered during the ARP could significantly enhance the contractility of myocardium safely, suggesting that CCM stimulation is a novel potent method for contractility modulation.

The purpose of this study was to investigate the changes of protein kinase Cα (PKCα) and cyclin D1 expressions in pulmonary arteries from smokers with normal lung function and smokers with mild to moderate chronic obstructive pulmonary disease (COPD). The peripheral lung tissues were obtained from 10 non-smokers with normal lung function (non-smoker group), 14 smokers with normal lung function (smoker group), 11 smokers with mild to moderate COPD (COPD group). The morphological changes of pulmonary arteries were observed by HE-staining. The expressions of α-smooth muscle actin (α-SMA), proliferating cell nuclear antigen (PCNA), PKCα and cyclin D1 proteins in pulmonary artery smooth muscle cells (PASMCs) were immunohistochemically determined. The percentages of PCNA-positive cells were taken as the smooth muscle cells proliferation index (PI). The mRNA expressions of PKCα and cyclin D1 in PASMCs were evaluated by real-time fluorescence PCR. Morphometrical analysis showed that the ratio of pulmonary artery wall area to total area (WA%) in smoker group and COPD group was significantly greater than that in non-smoker group (P<0.01). The PASMCs proliferation index in smoker group and COPD group was significantly higher than that in nonsmoker group (P<0.01). The protein levels of PKCα and cyclin D1 in PASMCs were significantly increased in smoker group and COPD group as compared with non-smoker group (P<0.01). The mRNA expressions of PKCα and cyclin D1 in PASMCs were significantly elevated in smoker group and COPD group as compared with non-smoker group (P<0.01). Significant correlations were found between PKCα protein and WA% or PI (P<0.01). Correlations between cyclin D1 protein and WA% or PI also existed (P<0.01). The expression of PKCα was positively correlated with the expression of cyclin D1 at both protein and mRNA levels (P<0.01). In conclusion, increased expressions of PKCα and cyclin D1 might be involved in the pathogenesis of abnormal proliferation of PASMCs in smokers with normal lung function and smokers with mild to moderate COPD.

Little is reported about the role of PTEN gene in the progression and prognosis of GISTs. This study examined the clinical implications of the tumor suppressor gene PTEN as a prognostic factor in the GISTs. Immunohistological staining and immunoblotting were employed to examine the PTEN protein expression, and its association with clinical measures. Clinicopathological features were reviewed by a retrospective examination of medical records. Reduced PTEN expression was significantly associated with tumor diameter, mitotic figure count, metastasis and pathological stage of tumor (P<0.05), and was not correlated with age, gender and tumor location (P>0.05). The 3-year survival rate of the patients with reduced PTEN expression was significantly lower than those with high PTEN expression (P<0.01). These results suggest that the expression of PTEN gene was significantly linked with the progression and metastasis of GISTs and it is an independent prognostic factor.

This study examined the mRNA expression of NALP3 in the spleen of the mice with hypersplenism due to portal hypertension (PH). The mouse hypersplenism models were established by oral administration of tetrachloromethane (2 mL/kg/week for 12 weeks by oral gavage). All the mice were randomly divided into a control group and an experimental group. The blood routine test was conducted, spleen index was calculated and spleen was histologically examined. Portal vein sera were taken for detection of the level of uric acid. The mRNA expressions of NALP3 and IL-1β in the spleen were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). The results showed that the platelet count was significantly lower in the experimental group [(674±102)×10⁹/L] than in the control group [(1307±181)×10⁹/L] (P<0.05), while the spleen index was significantly higher [(9.83±1.36) μg/g] in the experimental group than in the control group [(4.11±0.47) μg/g] (P<0.05). The histopathological changes of spleen followed the pattern of congestive splenomegaly. No significant difference was found in the uric acid level in the portal vein between the control group and the experiment group. The mRNA expressions of NALP3 and IL-1β were up-regulated significantly in the spleen in the experimental group as compared with those in the control group (P<0.05). It was concluded that NALP3 and IL-1β may play important roles in the pathogenesis of hypersplenism.

KLD-12 peptide with a sequence of AcN-KLDLKLDLKLDL-CNH₂ was synthesized and its biocompatibility was assessed in animals. Rabbit MSCs were cultured in the hydrogel for 2 weeks. Live cells were counted by using Calcein-AM/PI fluorescence staining. MTT was employed to assess the viability of MSCs cultured in KLD-12 peptide solution of 0.01%, 0.03%, and 0.05%. Hemolysis test, skin irritation test and implantation test were conducted to evaluate its biocompatibility with host tissues. Our results demonstrated that the MSCs in hydrogel grew well and maintained round shape. Cell survival rate was 92.15% (mean: 92.15%±1.17%) at the 7th day and there was no difference in survival rate between day 7 and day 14. Cell proliferation test showed that the A value of the KLD-12 solutions was not significantly different from that of control groups (complete culture media) (P>0.05) at the 24th and 48th h. The hemolysis rate of KLD-12 solution was 0.112%. Skin irritation test showed that the skin injected with KLD-12 solution remained normal and the score of skin irritation was 0. The histological examination with HE staining exhibited that the skin layers were clear and there was no infiltration with neutrophilic granulocytes and lymphocytes. It is concluded that KLD-12 peptide hydrogel had a good biocompatibility with host rabbit and MSCs, and KLD-12 peptide hydrogel can provide an appropriate microenvironment for MSCs.

This study examined the effect of IKVAV peptide nanofiber on proliferation, adhesion and differentiation into neurocytes of bone marrow stromal cells (BMSCs). IKVAV Peptide-amphiphile was synthesized and purified. Then, hydrogen chloride was added to the diluted aqueous solutions of PA to induce spontaneous formation of nanofiber in vitro. The resultant samples was observed under transmission electron microscope. BMSCs were cultured with IKVAV peptide nanofiber. The effect of IKVAV nanofiber on the proliferation, adhesion and induction differentiation of BMSCs was observed by inverted microscopy, calcein-AM/PI staining, cell counting and immunofluorescence staining. The results demonstrated that IKVAV peptide-amphiphile could self-assemble to form nanofiber gel. BMSCs cultured in combination with IKVAV peptide nanofiber gel grew well and the percentage of live cells was over 90%. IKVAV peptide nanofiber gel exerted no influence on the proliferation of BMSCs and could promote the adhesion of BMSCs and raise the ratio of neurons when BMSCs were induced to differentiate into neurocytes. It is concluded that BMSCs could proliferate and adhere well and yield more neurons during when induced to differente into neurocytes on IKVAV peptide nanofiber gel.

This study examined the effect of GHRP-6, a known GHSs receptor agonist, on the phosphorylation of cAMP-responsive element-binding protein (CREB) and the underly mechanism. GH3 cells were cultured and subjected to different treatments as follows: GHRP-6, GHRP-6 plus GHRH, phorbol ester (PMA), an activator of PKC, alone or in combination with GHRP-6, Gö6983, a general inhibitor of PKCs, in the presence or absence of GHRP-6, rottlerin, an inhibitor of PKCs, alone or plus GHRP-6. The cells were transiently transfected with PKCσ-specific siRNA and then treated with GHRP-6. GH level was measured by enzyme-linked immunosorbent assay (ELISA). The expression of phosphor-CREB, PKCσ, PKCθ and phosphor-PKCσ was determined by Western blotting. The results showed that GHRP-6 stimulated GH secretion in both time- and dose-dependent manners and enhanced the effect of GHRH on GH secretion. GHRP-6 was also found to induce CREB phosphorylation. Moreover, GH secretion was enhanced by the PKC activator PMA and reduced by the PKC inhibitors (Gö6983, rottlerin) and knockdown of PKCσ. PKCσ could be activated by GHRP-6. It is concluded that PKC, especially PKCσ, mediates CREB phosphorylation and GHRP-6-induced GH secretion.

To examine the changes in matrix metalloproteinase-2 (MMP-2) and -9 (MMP-9) in the development and progression of endometriosis, real time quantitative polymerase chain reaction, enzyme-linked immunoabsorbent assay and gelatin zymography were employed to determine the mRNA and protein levels and activities of MMP-2 and MMP-9 from the first day to the 21^st day after the induction in mice with induced endometriosis (experimental group) and sham-operated animals (controls). The results showed that the mRNA and protein levels and activities of the MMP-2 and MMP-9 were significantly increased on the first day after the induction and the level of MMP-2 stayed at a level higher than that in the control group. MMP-9 had two or three peaks during the 21 days, taking place at day 1, 4 and 15. It is concluded that the changes in the MMP-2 and MMP-9 might be involved in pathogenesis of endometriosis.

In our previous study, we identified a novel testis-specific expressed gene 2 (TSEG-2) from mouse testis. To further investigate its functions, 35 male Balb/c mice (8 weeks old) were divided into cryptorchidism group (n=20), sham group (n=10), and control group (n=5). In cryptorchidism group, the right testes were anchored to the inner lateral abdominal wall. In situ hybridization (ISH) was applied to measure the localization of TSEG-2 in mouse testis. Real-time quantitative PCR was performed to detect the expression of TSEG-2 gene. Meanwhile, under the mediation of polyethylenimine (PEI), the recombinant vector pEGFP-TSEG-2 (n=5) or empty vector (mock, n=5) was transfected into the testis of male mice. The transfection efficiencies were measured under a fluorescence microscope. The apoptosis of spermatogenic cells was detected by terminal deoxynuleotidyl-mediated nick end labeling (TUNEL). The results showed that TSEG-2 was expressed in convoluted seminiferous tubules, more precisely, in spermatogonia and spermatocytes. As compared with sham and control groups, the TSEG-2 transcription was significantly enhanced (P<0.05) and was correlated with apoptosis of spermatogenic cells in cryptorchid testes (P<0.05). PEI was efficient in mediating transfection of TSEG-2 into seminiferous tubules of testis. One week post-transfection, intratesticular injection of TSEG-2 resulted in increased apoptosis of spermatogenic cells in vivo (P<0.05). These results indicate that TSEG-2 may participate in the apoptosis of spermatogenic cells and the pathogenesis of cryptorchidism.

In this study, the vaporization ratio of the 2-μm laser in the prostatic tissue with benign prostatic hyperplasia was examined in vitro, to explore a technique to estimate the clearance rate of prostatic tissue during the transurethral vaporesection of the prostate. A total of 9 fresh prostatic tissue specimens were obtained by open surgery and the wet weight of the prostatic tissue were measured immediately after the sample collection. Under the simulated conditions of transurethral vaporesection of the prostate by 2-μm laser, each prostate gland was completely vaporesected into fragments with a diameter of less than 1.0 cm in vitro. After the vaporesection, the whole fragments of prostatic tissue were collected and measured. Then the lost weight of prostatic tissue, the weight of the collected prostatic tissue and the ratio of the lost weight of prostatic tissue to the wet weight of the prostate glandular organ specimen were calculated. The correlation between the weight of collected prostatic tissue and the weight of the whole glandular organ was analyzed. All the experimental procedures were carried out by one operator. Wet weight of the prostatic gland specimen and the weight of the harvested prostatic tissues after the procedure were recorded. With respect to the wet weight of prostate gland specimen, the percentage of the weight of collected prostatic tissue was (34.45±1.51) %, and the percentage of the lost weight of prostatic tissue was (65.55±1.51)%. Satisfactory linear relationship was observed between the weight of collected prostatic tissue and the wet weight of prostate gland specimen [y=3.245x−6.475 (t=15.097, P=0.000)]. It is concluded that under the simulated conditions of transurethral vaporesection of the prostate by 2-μm laser, the vaporization ratio of prostatic tissue can be calculated on the basis of the weight of collected prostatic tissue, and thereby the clearance of prostatic tissue during the formal operation by 2-μm laser could be quantitatively determined.

Astrocytes play a major role in the reactive processes in response to neuronal injuries in the brain. Excessive gliosis is detrimental and can contribute to neuronal damage. CD81 (TAPA), a member of the tetraspanin family of proteins, is upregulated by astrocytes after traumatic injury to the rat central nervous system (CNS). To further understand the role of CD81 in the inhibition of astrocytes, we analyzed the effects of a CD81 antibody, on cultured rat astrocytes. The results indicated that the effect worked in a dose-dependent manner with certain dosage range. It, however, reached a dosage equilibrium at a high dosage. Furthermore, anti-CD81 antibody remarkably inhibited the proliferation of astrocytes after incubation with astrocytes for different periods of time and the effect presented a time-dependent fashion. However, anti-CD81 antibody substantially inhibited the proliferation of astrocytes at low density and middle density but slightly inhibited the proliferation of astrocytes at high density, suggesting that the effect was positively correlated with the proliferative ability of astrocytes. Finally, the cell cycle of astrocytes exposured to anti-CD81 antibody was arrested in S phase at the initial stage and at G₀/G₁ phase over time. These findings indicated that CD81 exert significant inhibitory effect, dose-dependently and time-dependently, on the proliferation of astrocytes and the effect is positively correlated with the proliferative capability of astrocytes.

Recent evidence has suggested that Akt2 plays an important role in the protection of cells from paclitaxel (PTX)-induced apoptosis and control of the cell cycle. In addition, some scholars suggested that the PTX sensitivity depends on a functional spindle assembly checkpoint. In the present study, we investigated the role of the Akt2/Bub1 cross-talking in apoptosis and cell cycle after exposure of the A2780 ovarian cancer cells to paclitaxel (PTX). Recombinant expression plasmid WT-Akt2 was transfected into A2780 cells by lipofectamine2000, and then the expression level of Akt2 gene was detected by using RT-PCR and Western blotting. Cell apoptosis and cell cycle were detected by flow cytometry and Hoechst 33342 staining after treatment with PTX. Moreover, we compared the expression level of Bub1 in different groups by Western blotting. Our study showed that up-regulation of Akt2 contributed to A2780 ovarian cancer cells overriding PTX-induced G₂/M arrest, and inhibited Bub1 expression. Our findings might shed light on the molecular mechanism of PTX-induced resistance in ovarian cancer and help develop novel anti-neoplastic strategies.

This study evaluated the efficacy and safety of “J”-shaped uterine incision for caesarean section for patients diagnosed with placenta previa. A total of 55 consecutive cases of placenta previa treated in Union Hospital were retrospectively analyzed over a period of two years and 10 months. The subjects were divided into two groups with respect to the uterine incision. Twenty-four pregnant women with placenta previa who were indicated for caesarean section underwent the procedure using a new “J”-shaped uterine incision and 31 pregnant women with placenta previa received caesarean section that used the traditional transverse incision. The two groups were compared in terms of operation time, estimated blood loss, infant expulsion time, exhaust time and postoperative recovery. Meanwhile, comparison was also made in neonatal clinical data between the two groups. Compared with the “J”-shaped incision group, the traditional incision group had a lower Apgar scores (P<0.05). However, there existed no statistically significant differences in the overall time of operation and postoperative period of breaking wind (P>0.05). It is concluded that, with caesarean section for placenta previa patients, the “J”-shaped uterine incision significantly decreases intraoperative blood loss and facilitates the fetal delivery.

To investigate the effect of Dachengqi decoction on NF-κB p65 expression in lung of rats with partial intestinal obstruction and the underlying mechanism, 30 SD rats were randomly divided into three groups: sham-operation group, model group and Dachengqi decoction treatment group (Dachengqi group), with 10 animals in each group. The models were made by partially ligating their large intestines outside the body. The pathological changes were analyzed by HE staining. The expression of NF-κB p65 in rats lung were measured by using real-time polymerase chain reaction and immunohistochemistry respectively. Moreover, the expression of caveolin-1 in rats lung was also measured to. Increased edema, interstitial thickening, hemorrhage, and infiltration of inflammatory cells were found in the model group. In contrast, this change was significantly reduced in Dachengqi group as compared with model group. In addition, the up-regulated caveolin-1 and NF-κB p65 were also suppressed by Dachengqi decoction in lung of rats with partial intestinal obstruction. We are led to concluded that the caveolin-1-NF-κB pathway plays an important role in the development of lung injury of rats with partial intestinal obstruction and Dachengqi decoction could down-regulate the expression of caveolin-1 and NF-κB p65 in lung of rats with partial intestinal obstruction.

Th2 cytokines play a pivotal role in the pathogenesis of allergic rhinitis. To investigate the effect of p38 mitogen-activated protein kinase (MAPK) on the production of Th2 cytokines such as IL-4 and IL-5 in allergic rhinitis, a model of allergic rhinitis was established in SD rats. The expression level of p38 MAPK mRNA in PBMCs was detected by means of real time quantitative RT-PCR. The p38 MAPK activity in PBMCs was detected by Western blotting. PBMCs were cultured with various concentrations of p38 MAPK inhibitor SB 239063 or without the treatment, and then IL-4, IL-5 levels of the supernatant were determined by using sandwich ELISA. The results showed that mRNA expression and activity of p38 MAPK in PBMCs were significantly higher in allergic rhinitis rats than in control rats (P<0.05). The p38 MAPK inhibitor SB 239063 decreased the production of IL-4 and IL-5 in a dose-dependent manner. It is concluded that p38 MAPK plays an important role in the pathogenesis of allergic rhinitis which is associated with Th2 cytokines release.

In this study, the sterilizing effect of atmospheric pressure nonequilibrium plasmas (APNPs) on Neisseria gonorrhoeae (N. gonorrhoeae) was preliminarily examined and the possible mechanisms were explored. N. gonorrhoeae FA1090, FA19 and MS11 were treated by APNPs and their survival rate was analyzed by using CFUs counting and structurally studied by laser scanning confocal microscopy. The morphological changes of bacterial cell membrane and wall were studied under TEM. Our results showed that APNPs had strong sterilizing effect on N. gonorrhoeae. The survival rate of MS11 in N. gonorrhoeae liquid medium was 60.65% after disinfection with the APNPs for 5 min, whereas, the survival rate of FA19 was 92.60% and the rate of FA1090 was 96.40%. The survival rate of MS11 was 21.13% after exposure to APNPs for 6 min, whereas the survival rate of FA19 was 31.60% and the rate of FA1090 was 91.00%. N. gonorrhoeae was structurally damaged after treatment with APNPs. It is concluded that APNPs is able to effectively and quickly kill the N. gonorrhoeae, and the killing effect is related to the architectural damage of cell membrane.

This study investigated the growth-regulating effects of progesterone (Prog) on nPR-negative malignant melanoma cells and the possible mechanisms. A375 and A875 cells were cultured and treated with Prog of different concentrations. For signal transduction pathway studies, the cells were pretreated with Prog receptor antagonist (RU486, 1×10⁻⁷ mol/L) or MAPK inhibitor (U0126, 5×10⁻⁶ mol/L) for 1 h and then co-incubated with prog (10⁻⁹ mol/L) for another 24 h. Indirect immunofluorescence assay, MTT, flow cytometry and Western blotting were used for assessing the nPR expression, cell growth, cell apoptosis and ERK1/2 Phosphorylation, respectively. Our results showed that lower progesterone concentration promoted the proliferation of both A375 and A875 cells, but this growth-stimulatory effect decreased at progesterone concentration of 1×10⁻⁷ mol/L or higher. The response could be abolished by MAPK inhibitor U0126, but could not be blocked by progesterone antagonist RU486. Flow cytometry exhibited that high concentration (⩾1 × 10⁻⁷ mol/L) progesterone increased the apoptosis of the two cells in a dose-dependent manner. The level of ERK1/2 phosphorylation was increased by a lower progesterone concentration, but reduced by a higher concentration (1×10⁻⁶ mol/L). These results suggest progesterone exerts growth-regulating effects on nPR-negative tumor cells through a non-genomic mechanism.

Corneal opacity is one of the most commonly used parameters for estimating postmortem interval (PMI). This paper proposes a new method to study the relationship between changes of corneal opacity and PMI by processing and analyzing cornea images. Corneal regions were extracted from images of rabbits’ eyes and described by color-based and texture-based features, which could represent the changes of cornea at different PMI. A KNN classifier was used to reveal the association of image features and PMI. The result of the classification showed that the new method was reliable and effective.

In this study, norcanthridin (NCTD)-encapsulated liposomes were modified with a novel murine anti-human CD19 monoclonal antibody 2E8 (2E8-NCTD-liposomes) and the targeting efficiency and specific cytotoxicity of 2E8-NCTD-liposomes to CD19⁺ leukemia cells were evaluated. BALB/c mice were injected with 2E8 hybridoma cells to obtain 2E8 monoclonal antibody (mAb). NCTD-liposomes were prepared by using film dispersion method. 2E8 mAbs were linked to NCTD-liposomes using post-incorporation technology. Flow cytometry showed that the targeting efficiency of purified 2E8 mAbs on CD19⁺ Nalm-6 cells was 99.93%. The purified 2E8 mAbs were conjugated with NCTD-liposomes to prepare 2E8-NCTD-liposomes whose targeting efficiency on CD19⁺ Nalm-6 was also 95.82%. The average size of 2E8-NCTD-liposomes was 118.32 nm in diameter. HPLC showed that the encapsulation efficiency of NCTD was 46.51%. When the molar ratio of 2E8/Mal-PEG₂₀₀₀-DSPE reached 1:50, we obtained the liposomes with 9 2E8 molecules per liposome. The targeting efficiency of 2E8-NCTD-liposomes on CD19⁺ leukemia cells was significantly higher than that on CD19-leukemia cells. Similarly, the targeting efficiency of the immunoliposomes was also higher than that of the NCTD-liposomes on CD19⁺ leukemia cells. Those results were consistent with those observed by laser scanning confocal microscopy. 3-(4, 5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay demonstrated that 2E8-NCTD-liposomes specifically killed Nalm-6 cells in a dose- and time-dependent manner. The viability of Nalm-6 cells treated by 2E8-NCTD-liposomes was significantly lower than that of Molt-3 cells and it was also significantly lower than that of Nalm-6 cells treated with the same concentration of NCTD-liposomes or free NCTD. We are led to concluded that 2E8 antigen can serve as a specific targeting molecule of B lineage hematopoietic malignancies for liposome targeting, and 2E8-NCTD-liposomes can be used as a new and effective means for the treatment of B lineage hematopoietic malignancies.

To evaluate lesion detection of MRI in knee joint osteoarthritis in patients with symptoms of pain, the correlation between MRI findings and varying degrees of reported pain was assessed. Twenty-eight patients (31 knees) with osteoarthritis were recruited for this study. The degree of knee pain was assessed by VRS scores. The knees were evaluated by plain film radiograph utilizing Kellgren-Lawrence scores. Multiple MR sequences were performed on a 1.5T MR-system, including sagittal and coronal dual fast spin echo (TR/TE 3660/11/120 ms, slice thickness 5 mm), coronal spin echo T1-weighted (TR/TE 360/9 ms, slice thickness 5 mm), sagittal fat saturated 3D-spoiled gradient-recalled echo (TR/TE 50/6 ms; slice thickness 1.5 mm; flip angle 40°), and 3D steady-state free precession (TR/TE 6/2.2 ms; slice thickness 1.6 mm; flip angle 30°) pulse sequences for the purpose of detecting abnormities of cartilage, menisci, the anterior cruciate ligaments, bone marrow edema-like lesions, osteophytes, synovitis, and joint effusions. MR findings were compared with the degree of pain using Fisher exact test with P values less than 0.05 indicating a statistically significant difference. The results showed that, of the 31 knees evaluated, mild pain was reported in 11 and severe pain in the remainder. Kellgren-Lawrence scores of all 31 evaluated OA knees were as follows: grade 1 lesions (n=6), grade 2 lesions (n=14), grade 3 lesions (n=8), and grade 4 lesions (n=3). Articular cartilaginous defects were found in 37.1% of knees. Abnormalities of the menisci and anterior cruciate ligaments, bone marrow edema-like lesions, osteophytes, synovitis, and joint effusions were detected in 32.3%, 38.7%, 45.2%, 100%, 15.1% and 67.7% of knees, respectively. Of these variables, only the differences in prevalence of joint effusions were significantly different in the mild and severe pain groups (P=0.004). It is concluded that MRI evaluates the entire joint structure of the osteoarthritic knee, demonstrating abnormalities of the cartilage, menisci, and anterior cruciate ligaments as well as bone marrow edema-like lesions, osteophytes, synovitis, and joint effusions. The difference in pain grading between OA patients reporting mild and severe degrees of pain is related to the presence of joint effusion.

The chemical constituents of fistular onion stalk obtained by supercritical CO₂ extraction were separated and purified by silica gel and sephadex LH-20 gel column chromatography and the preparative TLC method and four flavonoids were obtained. On the basis of the spectral data, they were structurally identified as (+)-catechin, (−)-epicatechin, astragalin, and 3-O-β-D(2-O-β-D-glucopyranosyl)-glucopyranosides of kaempferol.

This study examined the effects of exercise on behavior and peripheral blood leukocyte apoptosis in a rat model of chronic fatigue syndrome (CFS). Thirty-six healthy male Sprague-Dawley rats were equally randomized into 3 groups: the control group, CFS model group and the exercise group in terms of body weight. A total of 25 rats entered the final statistical analysis due to 11 deaths during the study. CFS model was established by subjecting the rats in CFS model group and exercise group to electric shock, chronic restraint stress and cold water swim. Besides, rats in the exercise group took running wheel exercise. After a week of conditioning feeding, model construction and running wheel exercise were performed simultaneously, and lasted for 23 consecutive days. The behavior experiments, including running wheel exercise, open-field test, tail suspension test and Morris water maze test, were conducted, either before or after the model establishment. Rats were sacrificed and peripheral blood was obtained for the assessment of lymphocyte apoptosis index by flow cytometry (FCM). It was found that as compared with those in the control group, the weight of the rats was decreased obviously (P<0.01), the mobility time in the open-field and the tail suspension tests was shortened significantly (P<0.01), the time to locate the platform was enhanced (P<0.01) and the cell apoptosis index was increased substantially (P<0.01) in the CSF model group. Meanwhile, in comparison to the model group, the behavior in the open-field and the tail suspension tests was improved significantly (P<0.05), and the apoptosis index decreased remarkably (P<0.01) in the exercise group. It is concluded that sport intervention can prevent lymphocyte apoptosis and improve animal behavior rather than the memory.