Effectiveness of Hair Care Products Containing Placental Growth Factor for the Treatment of Postpartum Telogen Effluvium

BACKGROUND: Postpartum telogen effluvium refers to a phenomenon in which some hair in the growth phase progresses rapidly to the resting phase, which leads to excessive hair loss. This causes a high level of psychological stress. Therefore, an increasing number of women are seeking treatment for this condition. METHODS: The subjects of this study were postpartum women in the age range of 20 to 40 years who visited a university hospital between June 2015 and May 2016. Seven patients out of a total of 25 subjects were excluded, and their final follow-up visits were not performed because they found it difficult to return for the follow-up. After screening before delivery, the subjects were provided with hair care products. They visited the hospital 1 week, 1 month, and 3 months after giving birth. During each visit, the hair density and thickness were measured by photographing with a camera and using Folliscope® (Aram Huvis Corporation, Seoul, Korea). RESULTS: The hair thickness at the V-point improved from 0.089 µm at the baseline to 0.094 µm after using the shampoo for 3 months (P=0.028), and the hair density at the P-point increased significantly, from 75.24/cm² at the baseline to 81.33/cm² after using the shampoo for 3 months (P<0.001). CONCLUSIONS: In this study, a shampoo and a tonic in which the main material was horse placental growth factor combined with various materials, such as pumpkin extract, panthenol, and niacinamide, were clinically applied.

Effectiveness of Hair Care Products Containing Placental Growth Factor for the Treatment of Postpartum Telogen Effluvium

BACKGROUND: Postpartum telogen effluvium refers to a phenomenon in which some hair in the growth phase progresses rapidly to the resting phase, which leads to excessive hair loss. This causes a high level of psychological stress. Therefore, an increasing number of women are seeking treatment for this condition. METHODS: The subjects of this study were postpartum women in the age range of 20 to 40 years who visited a university hospital between June 2015 and May 2016. Seven patients out of a total of 25 subjects were excluded, and their final follow-up visits were not performed because they found it difficult to return for the follow-up. After screening before delivery, the subjects were provided with hair care products. They visited the hospital 1 week, 1 month, and 3 months after giving birth. During each visit, the hair density and thickness were measured by photographing with a camera and using Folliscope® (Aram Huvis Corporation, Seoul, Korea). RESULTS: The hair thickness at the V-point improved from 0.089 µm at the baseline to 0.094 µm after using the shampoo for 3 months (P=0.028), and the hair density at the P-point increased significantly, from 75.24/cm² at the baseline to 81.33/cm² after using the shampoo for 3 months (P<0.001). CONCLUSIONS: In this study, a shampoo and a tonic in which the main material was horse placental growth factor combined with various materials, such as pumpkin extract, panthenol, and niacinamide, were clinically applied.

Botulinum Toxin Type A for Treatment of Masseter Hypertrophy: Volumetric Analysis of Masseter Muscle Reduction over Time

BACKGROUND: There has been increasing interest in facial contouring procedures throughout Asian countries. As such, botulinum toxin A injections for masseteric hypertrophy have become a common procedure provided to patients who desire non-surgical correction of a square-angled mandible. We published a retrospective review of our initial results and our technique and treatment protocol in 2005. We also completed a long-term follow-up of the results (average follow-up period of 4.28 years) and the efficacy of repeated injections in 2010. The purpose of the current study is to systematically evaluate the changes to the masseter muscle at weekly intervals to determine the physiologic effects of botulinum toxin A injection. METHODS: Eight patients were prospectively followed on a weekly basis after botulinum toxin A injection for masseteric hypertrophy. Eight patients were followed for 15 weeks and four patients were followed for 25 weeks. Changes in the thickness of the muscle were recorded and analyzed. RESULTS: A reduction in the muscle thickness was found during the clenching phase of the muscle in the first week followed by a reduction in thickness during the resting phase in the second week. The reduction in muscle thickness continued until the eleventh week after which there was a gradual, but incomplete, return of muscle thickness over the study period. CONCLUSIONS: There is a predictable, phasic reduction in muscle thickness after botulinum toxin A injection for masseteric hypertrophy. This reduction first occurs during the clenching phase followed by a concomitant reduction during the resting phase. Maximal size reduction occurs at 11 weeks followed by gradual muscle size recovery.

Over-expression of testis-specific expressed gene 1 attenuates the proliferation and induces apoptosis of GC-1spg cells / 华中科技大学学报（医学）（英德文版）

The effects of over-expression of testis-specific expressed gene 1 (TSEG-1) on the viability and apoptosis of cultured spermatogonial GC-1spg cells were investigated, and the immortal spermatogonial cell line GC-1spg (CRL-2053™) was obtained as the cell model in order to explore the function of TSEG-1. We transfected the eukaryotic vector of TSEG-1, named as pEGFP-TSEG-1 into cultured spermatogonial GC-1spg cells. Over-expression of TSEG-1 inhibited the proliferation of GC-1spg cells, and arrested cell cycle slightly at G0/G1 phase. Transfection of TSEG-1 attenuated the transcript levels of Ki-67, PCNA and cyclin D1. In addition, over-expression of TSEG-1 induced early and late apoptosis, and reduced the mitochondrial membrane potential of GC-1spg cells. Moreover, transfection of TSEG-1 significantly enhanced the ratio of Bax/Bcl-2 and transcript levels of caspase 9, and decreased the expression of Fas and caspase 8 in GC-1spg cells. These results indicated over-expression of TSEG-1 suppresses the proliferation and induces the apoptosis of GC-1spg cells, which establishes a basis for further study on the function of TSEG-1.

Resistance of leukemia KG1a cells with positive N-cadherin in phase G(0) against killing activity of VP16 / 中国实验血液学杂志

Drug resistance is an important character of leukemic stem cells. To explore the mechanism of the chemotherapy resistance of N-cadherin positive leukemia cells, the quiescent state of N-cadherin positive leukemia cells was determined by flow cytometry and the relationship of G(0) phase cell ratio with the chemotherapy resistance was analyzed. After KG1a cells were induced to enter cell cycle, the G(0) phase cell ratio and the sensitivity of cells to VP16 were determined. Finally the quiescent state and drug resistance properties of KG1a cells were determined after inhibiting N-cadherin-mediated cell-cell interaction by EGTA treatment. The results showed that the G(0) phase cell ratio in N-cadherin positive KG1a cells was higher than that in N-cadherin negative KG1a cells. After KG1a cells were induced to enter cell cycle, the G(0) phase cell ratio was decreased significantly and the sensitivity of KG1a cells to VP16 increased. Following EGTA treatment for 24 hours, the G(0) phase cell ratio decreased and the drug-sensitivity was enhanced significantly. It is concluded that N-cadherin-mediated adhesion keeps N-cadherin positive leukemia cells in quiescent state of G(0) phase, thus protect these leukemia cells against VP16 chemotherapy.

Biosorption of Cr [VI] by resting cells of Fusarium solani

Chromium is one of the toxic heavy metals which exists in nature as stable hexavalent and trivalent forms. The hexavalent form of chromium is more toxic than trivalent chromium as it persists indefinitely in the environment complicating its remediation. The conventional physical and chemical treatment techniques used for the removal of Cr[VI] are expensive and highly energy intensive, moreover they produce harmful by-products, ultimate disposal of which again causes secondary pollution. Removal of Cr[VI] from aqueous solution using biological sources as biosorbent has assumed advantageous over the existing conventional physico-chemical techniques for the treatment of metal contaminated wastes. The present batch biosorption study was undertaken with an aim to examine the Cr [VI] removal potential of the resting cells of Fusarium solani [isolated from soil] from aqueous solution. The specific Cr [VI] removal decreased with increase in pH and increased with increase in initial Cr[VI] concentration, up to 500 mg/L. The specific Cr[VI] removal remained almost constant by increasing biomass concentration from 2.4 to 5.2 g/L. The studies also carried out by using the resting cells obtained from various stages of growth and the maximum specific Cr[VI] removal [60 mg/g] was achieved at 500 mg/L initial Cr[VI] concentration and by using cells [36 h old]. The Langmuir adsorption isotherm constants, Q[o] and b were observed to be 57.1 mg/L and 0.06 I 1/mg, respectively

Protein-energy malnutrition halts hemopoietic progenitor cells in the G0/G1 cell cycle stage, thereby altering cell production rates

Protein energy malnutrition (PEM) is a syndrome that often results in immunodeficiency coupled with pancytopenia. Hemopoietic tissue requires a high nutrient supply and the proliferation, differentiation and maturation of cells occur in a constant and balanced manner, sensitive to the demands of specific cell lineages and dependent on the stem cell population. In the present study, we evaluated the effect of PEM on some aspects of hemopoiesis, analyzing the cell cycle of bone marrow cells and the percentage of progenitor cells in the bone marrow. Two-month-old male Swiss mice (N = 7-9 per group) were submitted to PEM with a low-protein diet (4 percent) or were fed a control diet (20 percent protein) ad libitum. When the experimental group had lost about 20 percent of their original body weight after 14 days, we collected blood and bone marrow cells to determine the percentage of progenitor cells and the number of cells in each phase of the cell cycle. Animals of both groups were stimulated with 5-fluorouracil. Blood analysis, bone marrow cell composition and cell cycle evaluation was performed after 10 days. Malnourished animals presented anemia, reticulocytopenia and leukopenia. Their bone marrow was hypocellular and depleted of progenitor cells. Malnourished animals also presented more cells than normal in phases G0 and G1 of the cell cycle. Thus, we conclude that PEM leads to the depletion of progenitor hemopoietic populations and changes in cellular development. We suggest that these changes are some of the primary causes of pancytopenia in cases of PEM.

DAPT enhances the apoptosis of human tongue carcinoma cells / 国际口腔科学杂志·英文版

<p><b>AIM</b>To investigate the effect of DAPT (gamma-secretase inhibitor) on the growth of human tongue carcinoma cells and to determine the molecular mechanism to enable the potential application of DAPT to the treatment of tongue carcinoma.</p><p><b>METHODOLOGY</b>Human tongue carcinoma Tca8113 cells were cultured with DAPT. Cell growth was determined using Indigotic Reduction method. The cell cycle and apoptosis were analyzed by flow cytometry. Real-time PCR and Immuno-Fluorescence (IF) were employed to determine the intracellular expression levels.</p><p><b>RESULTS</b>DAPT inhibited the growth of human tongue carcinoma Tca8113 cells by inducing G0-G1 cell cycle arrest and apoptosis. The mRNA levels of Hairy/Enhancer of Split-1 (Hes-1), a target of Notch activation, were reduced by DAPT in a dose-dependent manner. Coincident with this observation, DAPT induced a dose-dependent promotion of constitutive Caspase-3 in Tca8113 cells.</p><p><b>CONCLUSION</b>DAPT may have a therapeutic value for human tongue carcinoma. Moreover, the effects of DAPT in tumor inhibition may arise partly via the modulation of Notch-1 and Caspase-3.</p>

The effect of p21 on transcription of survivin in hepatocellular carcinoma HepG2 cells and its regulation mechanism / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To observe the inhibitory effect of cyclin-dependent kinase inhibitor p21 on regulation of survivin transcription in human liver cancer HepG cells, and explore the related mechanisms.</p><p><b>METHODS</b>Doxorubicin (DOX) was used to treat HepG cells. Eukaryotic vector pEGFP-C2-p21 was transfected into HepG cells by lipofectamine and positive clones were screened out by G418. The mRNA expression of p21, p53 and survivin were detected by real-time fluorescent quantitative polymerase chain reaction (RQ-PCR). Flow cytometry was used to determine the cell cycle phases, and reverse transcription polymerase chain reaction (RT-PCR) was used to measure the levels of E2F-1 or p300.</p><p><b>RESULTS</b>After treatment with DOX, the expression of p53 and p21 was increased, whereas that of survivin was reduced during 24 hours of the treatment. After transfection the p21 level was 2100.1-fold or 980.9-fold enhanced in comparison with that in HepG2 cells or HepG2-pEGFP cells. Survivin level was markedly down-regulated to 0.5% or 0.6% relative to that in the other two groups, nevertheless, significant p53 changes were not observed. Overexpression of p21 resulted in G1/G0 phase arrest (F = 31.59, P < 0.01), meanwhile, E2F-1 mRNA or p300 mRNA were less expressed compared with that in the other controls (F(E2F-1) = 125.28, P < 0.05; Fp300 = 46.01, P < 0.01).</p><p><b>CONCLUSION</b>p21 could be a potential mediator of survivin suppression at transcription level in HepG2 cells, which might be through the block at G1/G0 phase and down-regulation of transcription factors E2F-1 and p300.</p>

Blockage of U251 cells in G0/G1 through MAPK signaling pathway by LRRC4 / 中南大学学报(医学版)

OBJECTIVE@#To explore the effect of LRRC4, a glioma suppressive gene, on blocking U251 cells in G0/G1 by MAPK signaling pathway.@*METHODS@#LRRC4 was transfected into U251 cells, and at 24 hour of post-transfection, cells were split at a 1:3 dilution, challenged with 500 microg /mL G418 and formed a stable transfected clone pool. RT-PCR, Northern blot and Western blot were used to identify the stable transfectants. ERK, JNK and P38 expression changes were analyzed by Western blot. FACS analysis, Luciferase reporter gene assay and Western blot were used to detect the cell cycle and cyclin D1.@*RESULTS@#LRRC4 down-regulated the expression of phosphorylated ERK2 and up-regulated the expression of total protein JNK2 (a key molecule of MAPK signaling pathway) and phosphorylated c-Jun. LRRC4 decreased the expression of mutation P53, cyclin D1 activation and its expression. U251 cells were blocked in G0/G1 by LRRC4.@*CONCLUSION@#LRRC4 can decrease JNK2, up-regulate the phosphoralated c-Jun, down-regulate mutant P53 and cyclin D1, and therefore block U251 cells in G0/G1.

Contragestazol (DL111-IT) inhibits proliferation of human androgen-independent prostate cancer cell line PC3 in vitro and in vivo / 亚洲男科学杂志(英文版)

<p><b>AIM</b>To evaluate the antiproliferative activity of contragestazol (DL111-IT) on the human prostate cancer cell line PC3 in vitro and in vivo and to elucidate its potential molecular mechanisms.</p><p><b>METHODS</b>The cell killing ability of DL111-IT was measured by the 3-(4,5-dimethylthia-zol,2-yl)-2,5-diphenyltetrazolium bromide (MTT) reagent assay method and the tumor xenograft model. The cell cycle was analyzed by flow cytometry and protein expression, including retinoblastoma (pRb), cyclin-dependent kinase 4 (CDK4) and cyclin D1, was detected by Western blotting.</p><p><b>RESULTS</b>DL111-IT exhibited high efficiency on cell growth inhibition of the human androgen-independent prostate cancer cell line PC3. The drug concentration that yielded 50% cell inhibition (IC50 value) was 9.9 mg/mL. In the PC3 tumor xenograft study, DL111-IT (1.25 mg/kg-20.0 mg/kg) given once a day for 10 days significantly inhibited tumor growth, with the inhibition rate ranging from 21% to 50%. Flow cytometric analysis indicated that DL111-IT could cause G1 arrest in the PC3 cell line, but not apoptosis. DL111-IT enhanced pRb expression and down-regulated CDK4 and cyclin D1 expression, suggesting that cell cycle regulation might contribute to the anticancer property of DL111-IT.</p><p><b>CONCLUSION</b>DL111-IT inhibits the proliferation of human androgen-independent prostate cancer cell line PC3 in vitro and in vivo by a cell cycle regulation pathway.</p>

Effects of 9-cis-retinoic acid on cell cycle and expression of cyclin D1 and cdk4 in lung cancer cells / 药学学报

<p><b>AIM</b>To study the effects of 9-cis-retinoic acid (9-cis-RA) on cell cycle and expression of cyclin D1 and cdk4 in lung cancer cells.</p><p><b>METHODS</b>9-cis-RA (1 x 10(-6) mol.L-1) was used to treat lung cancer cells for 24 h; Flow cytometry (FCM) was used to detect the percent of G0/G1 phase and S phase cells of three groups including blank control, DMSO control and 9-cis-RA groups; RT-PCR was used to analyze the expression changes of cyclin D1 and cdk4 before and after treatment with 9-cis-RA in lung cancer cells.</p><p><b>RESULTS</b>The percent of G0/G1 phase cells of 9-cis-RA groups was significantly higher than that of the control groups (P < 0.01 or P < 0.05) and the percent of S phase cells of 9-cis-RA groups was lower than that of the control groups (P < 0.01 or P < 0.05); the expression of cyclin D1 of PG, SPC-A1 and L78 cells was decreased (P < 0.01) and the expression of cdk4 of PG, A549 and L78 cells was also decreased (P < 0.01) after treatment with 9-cis-RA.</p><p><b>CONCLUSION</b>Most of the proliferation and the expression of cyclin D1 and cdk4 of PG, A549, SPC-A1 and L78 were inhibited by 9-cis-RA.</p>

Ciglitazone inhibits growth of lung cancer cells A549 in vitro and in vivo: an experimental study / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To study the inhibitory effects of ciglitazone, a synthetic ligand of peroxisome proliferator-activated receptors (PPAR), on human lung cancer growth in vitro and in vivo and its mechanisms.</p><p><b>METHODS</b>Human lung cancer A549 cells cultured in vitro were treated with different concentrations of ciglitazone. The proliferative activity and cell cycle of A549 cells were determined by MTT assay and flow cytometry. Expression of PPARgamma protein was detected by Western blot. A549 cells (1 x 10(6) cells/nude mouse) were inoculated subcutaneously into nude mice, which were randomly divided into two groups, 10 in each: control group (group A) and ciglitazone treated group (group B). When the tumors grew to a size with diameter around 1 cm, ciglitazone 100 microl (100 micromol/L) was intratumorally injected every other day in group B mice. A total of 15 injections were given. Mice in group A were similarly treated with normal saline. One month later, tumors were excised and weighed. Expression of cyclin D1 and p21 protein were detected by immunohistochemistry and Western blot.</p><p><b>RESULTS</b>Growth of A549 cells was significantly inhibited in group B in a dose-dependent and time-dependent fashion as compared with that in group A. Most of the ciglitazone-treated cells arrested in G(1)/G(0) phase and the expression of PPARgamma protein was markedly up-regulated. The tumor weights in group A was (2.79 +/- 0.33) g and that in group B was (1.51 +/- 0.40) g, with an inhibition rate of 47.0%. The expression level of cyclin D1 in group A was significantly higher than that in group B, while the expression level of p21 protein in group A was significantly lower than that in group B.</p><p><b>CONCLUSION</b>Ciglitazone can effectively inhibit the growth of human lung cancer A549 and induce its differentiation by cell cycle arrest via PPARgamma activation.</p>

Mechanism of Cultured Mouse Mesenchymal Stem Cell-Induced Suppression of Allogeneic Lymphocytes Proliferation / 대한혈액학회지

BACKGROUND: Mesenchymal stem cells (MSC) can be defined by their extensive in vitro self renewal capacity and multi-lineage differentiation potentiality. These cells possess in vitro immunosuppressive properties that appear not to be major histocompatibility complex (MHC) restricted. This study evaluated the immune suppressive effect of mouse MSC on mixed lymphocyte reaction (MLR), and the mechanisms were investigated. METHODS: MSC were obtained from BALB/c bone marrow and cultured in low-glucose DMEM media. The expression of surface antigens and cell cycle were analyzed by flow cytometry. The MSC-induced suppression was assessed by MLR and transwell culture. RESULTS: The BALB/c MSC constitutively expressed MHC class I and CD54 (ICAM-1) antigens but were negative for MHC class II, CD40, CD80 (B7-1) and CD106 (VCAM-1) antigens. MSC suppressed allogeneic C57BL/6 T lymphocytes proliferation by adding them to MLR in which C3H spleen cells were used as a stimulator. This inhibition was dependent on the dose of BALB/c MSC but independent of MHC. C57BL/6 T lymphocytes proliferation was still inhibited when BALB/c MSC were added in culture 3 days after starting of MLR. When MSC were separated from C57BL/6 T cells by using the transwell membrane, the suppression of immune response wasn't observed, which suggested that the suppressive effect was dependent on cell-cell contact between BALB/c MSC and C57BL/6 T cells. When C57BL/6 T lymphocytes were cultured with MSC, the percentage of C57BL/6 T cells in G0 phase increased from 51.8+/-7.66% to 77.2+/-7.39% compared with the case that only C57BL/6 T cells were cultured. When the C57BL/6 T cells were cultured with C3H spleen cells, most of C57BL/6 T cells were in G2/M (96.38+/-3.33%). But by the addition of MSC to MLR, the percentage of T cells in G2/M decreased to 33.0+/-9.66% while that of T cells in G0 increased to 66.2+/-7.46%. CONCLUSIONS: We concluded that the cell cycle of responder T lymphocytes in MLR is arrested at G0 phase by MSC.

Safety Assessment of Octylmethoxycinnamate, Butylmethoxydibenzoylmethane, and Octyltriazone Sunscreens by Human Repeated Insult Patch Tests to Compare the Shelanski and Maximization Tests / 대한피부과학회지

BACKGROUND: Human repeated insult patch tests (HRIPTs) are a final method for safety assessment of chemical ingredients. In the representative HRIPTs, the Shelanski and modified Draize require 200 participants, but the maximization and modified maximization tests require only 25. OBJECTIVE: To evaluate the safety of three sunscreen ingredients using the Shelanski and maximization methods. METHODS: Octylmethoxycinnamate, butylmethoxydibenzoylmethane, and octyltriazone (BASF) were prepared for the induction, as 25% ointment in white petrolatum base. After a 2-3 week resting phase, patch and photopatch tests were conducted, but pretreatment with SLS was only performed in the maximization test. The results were analyzed using the Chi-Square test. RESULTS: During the induction phase, there were only two (4%) weak positive reactions observed with the Shelanski method, whereas all 25 displayed strong or extremely positive reactions with the maximization method. Butylmethoxydibenzoylmethane displayed the most frequent elicitation reactions; the patch and photopatch tests displayed weak positive reactions in four (2%) and six (3%), and in one (4%) and two (8%), with the Shelanski and maximization tests, respectively. Taking into account two of the six reactors displayed positive reactions to petrolatum with the Shelanski test, the actual number of positive patch test reactions would be four (2%). The difference in results of the two methods was not statistically significant. CONCLUSION: Although it is not easy to conduct HRIPT on 200 subjects, and the results from the two tests were not significantly different, the reactions from the maximization tests were too severe to be recommended in humans.

P21(WAF1) inhibits the growth of leukemia cell line K562 and decreases its sensitivity to Vp16 / 中华血液学杂志

<p><b>OBJECTIVE</b>To explore the effect of p21(WAF1) on the proliferation and the sensitivity to Vp16 of leukemia cell line K562.</p><p><b>METHODS</b>A p21(WAF1) retroviral expression vector pLXSN-p21(WAF1) was constructed by FuGENE 6, pLXSN-p21(WAF1) and pLXSN-neo, and transfected into p21(WAF1) defect leukemia cell line K562. After selected with G418, K562-p21(WAF1) cell clones that stably expressed p21(WAF1) were isolated. The ectopic expressions of p21(WAF1) mRNA and protein in K562-p21(WAF1) were identified by RT-PCR and Western b1ot. The cell growth rate was tested by trypan blue dye, the cell cycle by FCM and the sensitivity to Vpl6 by cell count and MTT assay.</p><p><b>RESULTS</b>The expression of p21(WAF1) protein and mRNA could be detected in K562-p21(WAF1) cells. A strong inhibition of cell proliferation was observed in K562-p21(WAF1) cell as compared with that of the control. The cell number in G(0)/G(1) phase was remarkably increased. The sensitivity to Vpl6 decreased, the IC (50) of K562-neo cells was (56.4 +/- 6.5) microgram/ml, and that of K562-p21(WAF1) cells was (131.0 +/- 8.7) microgram/ml (P < 0.01).</p><p><b>CONCLUSION</b>p21(WAF1) can inhibit the proliferation of leukemia cell and decrease its sensitivity to Vp16.</p>

Study on the biological activity and molecular mechanism of IFNalpha on human myeloma cell line Sko-007 / 中华血液学杂志

<p><b>OBJECTIVE</b>To investigate the biological activity and molecular mechanism of interferon alpha (IFNalpha) on human myeloma cell line Sko-007.</p><p><b>METHODS</b>The effect of IFNalpha on the growth of Sko-007 cells was measured by MTT assay. Cells cycle distribution and the expression of two IL-6 receptor chains (IL-6R and gp130) on Sko-007 cell surface in the absence or presence of IFNalpha were monitored by FACS analysis. The activation state of protein kinase ERK, which is involved in Ras/MAPK signal transduction pathway mediating cell survival and proliferation, and the expression of anti-apoptotic Bcl-2 family proteins-Bcl-2, Bcl-x(L) and Mcl-1 in Sko-007 cells with or without IFNalpha were determined by immunoblot assay.</p><p><b>RESULT</b>IFNalpha arrested Sko-007 cell cycle progression. After stimulation with IFNalpha, an obvious increase in G(0)/G(1) phase (41.1%-->84.1%) and decrease in S phase (57.1%-->13.3%) of Sko-007 cell cycle distribution can be observed. Moreover, the proliferation of Sko-007 cells was dramatically inhibited in the presence of IFNalpha, with a maximal inhibitory rate up to 88%. In addition, the expression of gp130 on cell surface, the activation of protein kinase ERK and the expression of Bcl-2 and Bcl-x(L) were all down-regualted in IFNalpha-stimulated Sko-007 cells.</p><p><b>CONCLUSION</b>The inhibitory effect of IFNalpha on the proliferation of Sko-007 cells was mediated by gp130 down-regulation, degradation of Bcl-2 family anti-apoptotic proteins and inhibition of ERK activation.</p>

The influence of different nutritional support routes on the intestinal mucosal epithelial cell cycle in burned rats / 中华烧伤杂志

<p><b>OBJECTIVE</b>To explore the influence of different nutritional support routes on the intestinal mucosal epithelial cell cycle in burned rats.</p><p><b>METHODS</b>Sixty-six Wistar rats inflicted with 30% TBSA III degree burns on the back were employed as the model and were randomly divided into enteral feeding group (EF) and intravenously parenteral nutrition group (PN). Equal volume of nutritional support fluid containing predetermined equal amount of calories and nitrogen was applied via feeding or intravenously infusion through external jugular vein. The indices were observed on 6, 12, 24, 48 and 72 postburn hours (PBHs) with the reference to those in 6 normal rats. The intestinal epithelial cell cycle in jejunal and ileal mucous membrane was analyzed by flow cytometry. Western blotting method was employed in the examination of the expression of cyclin D1, E and that of cyclin dependent kinase (CDK)2 and CDK4.</p><p><b>RESULTS</b>(1) lntestinal mucosal epithelial G0/G1 ratio in jejunum in EF group was significantly lower than that in PN group at 72 PBHs (P < 0.05). While the ratio in ileum in EF was obviously higher than that in PN groups at 6, 12, 48 and 72 PBHs (P < 0.05). (2) The cell percentage of S phase in EF group was evidently higher than that in PN group (P < 0.05 - 0.01) at 48 and 72 PBHs. (3) Intestinal mucosal cyclin D1 expression increased significantly in EF group at 24 PBHs and in PN group at 48 PBHs (P < 0.05) and which in EF group was obviously higher than that in PN group at 72 PBHs (P < 0.05). (4) The expression of the intestinal mucosal cyclin E in EF group at 72 PBHs was evidently higher than the control value and that in PN group (P < 0.05). (5) The expression of CDK2 exhibited no obvious difference among PN,EF and control group (P < 0.05). The CDK4 expression in EF group increased obviously at 72 PBHs (P < 0.05).</p><p><b>CONCLUSION</b>Early postburn enteral feeding was beneficial to the progression of intestinal mucosal epithelial cell cycle and to the repairing and renovation of injured intestinal mucosal membrane. Cyclin and CDK might be important in the modulation of the intestinal mucosal epithelial cell cycle.</p>

Cell Cycle Analysis by Ki-67 Monoclonal Antibody in Acute Myelogenous Leukemia / 대한혈액학회지

BACKGROUND: Flow cytometric measurement of DNA can reveal G0/G1, S, G2/M phases of cell cycle, and BrdU labeling can determine the percentage of cells in active DNA synthesis. A monoclonal antibody (MoAb), Ki-67, recognizes a protein that is present only in the nucleus of cycling cells but absent in resting cells. We analyzed whether the resting and the proliferating fraction could be differentiated by double staining with Ki-67 MoAb and propidium iodide (PI), and observed the effects of GM-CSF on cell cycle in acute myelogenous leukemia (AML) cells by Ki-67 MoAb. METHODS: Blast cells were prepared from 9 AML patients. The cells were incubated for 48 hours with or without GM-CSF. Cells were stained with BrdU/PI and Ki-67/PI. Cell cycle was analyzed by flow cytometry. RESULTS: The average fraction of G0/G1, S, and G2/M phases was 84.6%, 10.9%, and 4.5 % by BrdU/PI and 87.8%, 8.6%, and 3.7% by Ki-67/PI, respectively. Ki-67/PI staining dis-criminated between G0 and G1 phases and the average was 71.5% and 16.3%, respectively. In cells incubated with GM-CSF, BrdU/ PI method showed that the average S phase fraction (SPF) significantly increased from 10.9 to 16.2% (P=0.01) and the fraction of G0/G1 phase decreased from 84.6% to 78.4% (P= .02). Ki-67/PI method showed that the median SPF significantly increased from 8.6% to 13.7% (P=0.05) and G0 fraction decreased from 71.5% to 58.1% (P=0.02) but G1 fraction increased from 16.3% to 22.3% (P=0.01). CONCLUSION: Cell cycle analysis by Ki-67 MoAb and PI in AML is rapid and simple. It is especially useful to determine the growth fraction and G0 fraction compared to BrdU/PI staining.