Objective To observe the efficacy of high-energy red light combined with human-like collagen dressing in treatment of facial corticosteroid addictive dermatitis.Methods Eighty-three patients with facial corticosteroid addictive dermatitis were divided into treatment group (42 cases) and control group (41 cases) by random digits table method.All patients in 2 groups were treated with ebastine 10 mg,once a day,and vitamin E cream,twice a day.At the same time,the patients in control group were given human-like collagen dressing,once a day in the first week,then 3 times/week.On the basis of control treatment,the patients in treatment group were irradiated with high-energy red light 10 min in face,2-3 times/week.The treatment of both groups lasted for 12 weeks.The symptoms,skin lesions and untoward reaction were observed after treatment of 4,8 and 12 weeks.Results After treatment of 4 weeks,there was no statistical difference in the effective rate between 2 groups (P ＞ 0.05).After treatment of 8 and 12 weeks,the effective rates in treatment group were significantly higher than those in control group [83.3％(35/42) vs.58.5％ (24/41),90.5％ (38/42) vs.65.9％ (27/41)],there were statistical differences (P ＜ 0.05).No untoward reaction was found in 2 groups.Conclusion High-energy red light combined with human-like collagen dressing is effective and safe in treatment of facial corticosteroid addictive dermatitis.

Objective To investigate the effect of Dexamethasone on microtubule - associated protein 1 light chain 3(LC3)expression of cells and neurons in cerebral cortex of juvenile Wistar rats with sepsis. Methods Models of juvenile Wistar rats with sepsis were established through cecal ligation and puncture(CLP). Totally 60 cases of 30 -day - old juvenile male Wistar rats were randomly divided into sham - operation group(10 cases),non - treated group (25 cases)and Dexamethasone group(25 cases). Twelve hours after CLP,rats in Dexamethasone group were injected with Dexamethasone(1 mg / kg)via tail vein every other day,with a total of 3 times. The same dose of saline was used in the non - treated group. All rats were killed at the age of 40 days. Expressions of LC3 and neuronal nuclei(NeuN)of cells in cerebral cortex of rats were detected by using immunofluorescence assay,and the number of positive cells was calculated by using image analysis system software. Expressions of LC3 - Ⅰ and LC3 - Ⅱ protein were measured by a-dopting Western blot. Results Three hours after CLP,rats appeared to be curled up and showed piloerection and shi-vering and the neurobehavioral score in non - treated group was significantly lower than that in sham - operation group (t = 9. 895,P = 0. 000). Twelve of 25 rats in Dexamethasone group died in 10 days after CLP(48% ),while 8 of 25 rats in non - treated group died(32% ),and the difference was not statistically significant between the 2 groups(χ2 =1. 333,P = 0. 248). The immunofluorescence staining and image analysis showed the percentage of LC3 positive cells in non - treated group was significantly increased(0. 606 7 ± 0. 030 1 vs 0. 353 3 ± 0. 025 8,t = 15. 644,P = 0. 000;0. 606 7 ± 0. 030 1 vs 0. 270 3 ± 0. 019 4,t = 22. 450,P = 0. 000). In non - treated group,the LC3 expression of cells in the cerebral cortex of rats was up - regulated,and the LC3 - Ⅱ/ LC3 - Ⅰ ratio was significantly higher than that in sham operation group and Dexamethasone group(0. 413 3 ± 0. 022 5 vs 0. 205 0 ± 0. 015 2,t = 18. 802,P = 0. 000;0. 413 3 ± 0. 022 5 vs 0. 185 0 ± 0. 023 5,t = 17. 206,P = 0. 000). The LC3 positive neurons in the cerebral cortex of rats were less in sham operation group and Dexamethasone group. The LC3 positive neurons were more in non - treated group than that in sham operation group and Dexamethasone group(0. 580 0 ± 0. 020 0 vs 0. 298 3 ± 0. 014 7,t =27. 783;P = 0. 000;0. 580 0 ± 0. 020 0 vs 0. 261 7 ± 0. 017 2,t = 28. 614;P = 0. 000). Conclusions The LC3 expres-sion of cells in the cerebral cortex of juvenile Wistar rats with sepsis was up - regulated,LC3 - Ⅱ/ LC3 - Ⅰ ratio in-creased,and the number of LC3 positive neurons also increased,while Dexamethasone could have inhibitory effect on them.

Objective:To detect the inhibitory effects of CAL-101, a selective inhibitor of phosphoinostitide-3'-kinase delta (PI3Kδ), on Burkitt's lymphoma cell line Raji and diffused large B-cell lymphoma cell line SUDHL-10 and elucidate its relative mechanism. Methods:Raji and SUDHL-10 cells were treated with various concentrations of CAL-101. Methyl thiazolyl tetrazolium (MTT) assay was performed to determine the inhibitory effect of CAL-101 on lymphoma cells, and cell apoptosis was measured by Annexin V/PI and DAPI staining. Migration assays were performed with transwell to detect the migration of lymphoma cells derived from the stromal cell line HK. Western blot was used to detect the phosphorylation status of the ERK pathway. MTT and CalcuSyn software analyses were preformed to detect whether or not combining CAL-101 with bortezomib induces synergistic cytoxicity. Results:CAL-101 at con-centrations of 5, 10, 15, and 20μmol/L inhibited cell proliferation in a dose-dependent manner. The proliferation rates of the Raji cells treated with 5, 10, 15, and 20μmol/L for 48 h were 29.17%± 1.23%, 38.15%± 1.51%, 46.46%± 1.78%, and 55.8%± 2.01%, respec-tively, which were significantly higher (P<0.05) than that of the control group (1.15% ± 0.02%). Similar results were found in the SUDHL-10 cells after treatment with CAL-101 (P<0.05). CAL-101 also exerted an apoptotic effect on the lymphoma cells. The apop-totic rates of the Raji cells treated with CAL-101 for 21 h were 22.69%± 3.83%and 49.96%± 7.36%, respectively, which were signifi-cantly higher (P<0.05) than that of the control group (5.23%± 2.04%). Similar results were found in the SUDHL-10 cells (P<0.05). Treatment with 5 and 10 μmol/L CAL-101 dose-dependently inhibited the migration activity of lymphoma cells to stromal cells (P<0.05). Western blot analysis showed that the expression level of ERK phosphorylation protein was significantly downregulated in the cells treated with CAL-101. A synergistic effect between CAL-101 and bortezomib was verified. That is, these two drugs can signifi-cantly inhibit the proliferation of lymphoma cells with CI values less than 1. Conclusion:The PI3Kδ-specific inhibitor CAL-101 sup-pressed the proliferation of Raji and SUDHL-10 cells, induced apoptosis, and inhibited stromal cell-derived migration. This inhibitory effect may be induced by blocking the ERK pathway. Overall, our study indicated that CAL-101 is a novel and potential agent in the therapeutic strategy against aggressive B-cell lymphoma.

OBJECTIVE: To show evidence of the autophagy in hippocampal nerve cells from rats with sepsis-associated encephalopathy (SAE) in vivo and to investigate the expression of microtubule-associated protein 1 light chain 3 (LC3). 
 METHODS: A rat model of sepsis was established by the cecal ligation and puncture (CLP). A total of 60 male Wistar rats (30 days old) were randomly divided into a sham group (n=10) and a CLP group (n=50). At 12 hours after CLP, the electroencephalogram (EEG) and somatosensory evoked potential (SEP) changes in rats were monitored and the neurobehavioral score was measured. According to the occurrence of SAE, the CLP group was further divided into an SAE(+) group and an SAE(-) group. Histopathological changes in hippocampus were observed by hematoxylin-eosin staining. An electron microscope was used to observe autophagosome formation and lysosome activation in the hippocampal nerve cells. Expressions of LC3-I and LC3-II protein were measured by Western blot. 
 RESULTS: Five of 50 rats in CLP group died in 12 hours after CLP. According to the low neurobehavioral score and abnormal EEG and SEP, 16 rats were diagnosed as SAE. The incidence of SAE was 35.56% (16/45). Compared with the sham group or the SAE(-) group, the frequency of α wave in SAE(+) group was significantly decreased at 12 hours after CLP, the δ wave increased, the P1 amplitude decreased, and the latency of SEP waves (P1 and N1) was prolonged (P<0.05). The morphology of hippocampal nerve cells was obvious in a status of edema. Pyramidal cells decreased significantly, even dissolved, and cell arrangement was in disorder in the SAE(+) group. But these cells were normal in the sham group and the SAE(-) group. The structure of hippocampal nerve cells was disordered, and the autophagy, granular matrix and square or rectangular crystals were found in the SAE(+) group. However, there was no autophagy both in the sham group and the SAE(-) group. LC3-II/LC3-I ratio in the hippocampal nerve cells was increased significantly at 12 hours after CLP in the SAE(+) group when compared with that in the sham or the SAE(-) group (P<0.05). 
 CONCLUSION There is autophagy in hippocampal nerve cells from rats with SAE and the LC3-II/LC3-I ratio is increased significantly.
Animals ; Autophagy ; Hippocampus ; Male ; Microtubule-Associated Proteins ; Neurons ; Rats ; Rats, Wistar ; Sepsis-Associated Encephalopathy

Objective To retrospectively explore the clinical symptoms ,diagnosis ,treatment and prognosis of posttransplant lymphoproliferative disorder (PTLD) after pediatric liver transplantation .Methods The diagnosis and treatment of PTLD were reviewed for 3 children recipient with living donor liver transplantation .Their primary diseases were biliary atresia ,glycogen storage disease type III and ornithine-transcarbamylase deficiency . All of them received FK506 for immunosuppression therapy . They were diagnosed as PTLD at 7 ,8 ,6 months post-operation respectively .Their major clinical manifestations were non-specific ,including fever ,diarrhea and anemia .Positron emission tomography/computed tomography (PET/CT) and ultrasound revealed enlarged mesenteric lymph nodes with neck lymphoadenopathy (n=2) . Pathological examinations of resected enlarged lymph nodes indicated post-transplantation lymphoproliferative disorder .One case was diffuse large B cell lymphoma and two of them belonged to preliminary EBER + . Results After a definite diagnosis ,there was one cycle of R-CHOP regimen (rituximab ,cyclophosphamide , pirarubicin ,vincristine ,dexamethasone) or 2 cycles of rituximab along with a .reduction of anti-rejection drug and they stayed in remission .Three were followed up for 37 ,39 and 20 months respectively from May 31 , 2019 . Currently transplanted liver function was stable and EBV viral load remained negative persistently .Conclusions This case highlights the complexity of clinical presentations and co-morbidities of PTLD . Reducing immunosuppressive agents and using rituximab plus chemotherapy can achieve a satisfactory efficacy for Epstein-Barr virus-related PTLD patients after pediatric liver transplantation .

The clinical performance and failure issues are significantly influenced by prosthetic malposition in unicompartmental knee arthroplasty (UKA). Uncertainty exists about the impact of the prosthetic joint line height in UKA on tibial insert wear. In this study, we combined the UKA musculoskeletal multibody dynamics model, finite element model and wear model to investigate the effects of seven joint line height cases of fixed UKA implant on postoperative insert contact mechanics, cumulative sliding distance, linear wear depth and volumetric wear. As the elevation of the joint line height in UKA, the medial contact force and the joint anterior-posterior translation during swing phase were increased, and further the maximum von Mises stress, contact stress, linear wear depth, cumulative sliding distance, and the volumetric wear also were increased. Furthermore, the wear area of the insert gradually shifted from the middle region to the rear. Compared to 0 mm joint line height, the maximum linear wear depth and volumetric wear were decreased by 7.9% and 6.8% at -2 mm joint line height, and by 23.7% and 20.6% at -6 mm joint line height, the maximum linear wear depth and volumetric wear increased by 10.7% and 5.9% at +2 mm joint line height, and by 24.1% and 35.7% at +6 mm joint line height, respectively. UKA prosthetic joint line installation errors can significantly affect the wear life of the polyethylene inserted articular surfaces. Therefore, it is conservatively recommended that clinicians limit intraoperative UKA joint line height errors to -2-+2 mm.
Humans ; Arthroplasty, Replacement, Knee ; Knee Joint ; Knee Prosthesis ; Mechanical Phenomena ; Polyethylene ; Osteoarthritis, Knee/surgery* ; Tibia/surgery* ; Biomechanical Phenomena

OBJECTIVETo investigate the proliferation inhibitory role and mechanism of PI3Kδ inhibitor CAL-101 on multiple myeloma (MM) cells, and to provide new therapeutic options for MM treatment.

METHODSMM cell lines U266 and RPMI8226 cells were treated with various concentrations of CAL-101. MTT assay and CalcuSyn software were performed to determine the inhibitory effect of CAL-101 and the synergistic effect with PCI- 32765, SAHA (suberoylanilide hydroxamic acid), BTZ (Bortezomib) on MM cells. The protein expression level of p-AKT, p-ERK, AKT, ERK and PI3Kδ processed by CAL-101 were analyzed by Western blot.

RESULTSCAL-101 at concentration of 15, 20, 25, 30 and 40 μmol/L could induce significant dose-dependent proliferation inhibition on U266 cells after treatment for 48 hours. The cell proliferation inhibition rates were (33.54 ± 1.23)%, (41.72 ± 1.78)%, (53.67 ± 2.01)%, (68.97 ± 2.11)% and (79.25 ± 1.92)%, respectively. Similar results were found in RPMI8226 cell line. Western blots showed high expression level of p-AKT, p-ERK, AKT, ERK and PI3Kδ in cell lines and MM primary cells. p-AKT and p-ERK protein expression levels were down-regulated significantly by CAL-101 treatment. Synergistic effect has been verified between CAL-101 and PCI-32765, SAHA and Bortezomib in U266 cell line, and PCI-32765, Bortezomib in RPMI8226 cell line with CI values less than 1.

CONCLUSIONCAL-101 could inhibit proliferation of MM cell lines. High levels of p-AKT, p-ERK, AKT, ERK and PI3Kδ protein expression were observed in both cell lines and primary cells. Down-regulation of p-AKT and p-ERK probably related with the mechanism of CAL-101 in MM cell proliferation inhibition. CAL-101 has significant synergistic effect with PCI-32765, SAHA and BTZ.

Boronic Acids ; Bortezomib ; Cell Line, Tumor ; Cell Proliferation ; Down-Regulation ; Humans ; Multiple Myeloma ; pathology ; Phosphatidylinositol 3-Kinases ; antagonists & inhibitors ; Protein Kinase Inhibitors ; pharmacology ; Purines ; pharmacology ; Pyrazines ; Pyrazoles ; Pyrimidines ; Quinazolinones ; pharmacology