Cell Line, Tumor ; Cell Proliferation ; drug effects ; Diterpenes, Kaurane ; pharmacology ; Humans ; Nasopharyngeal Neoplasms ; pathology

Abstract; Aim To explore the differences of 2,4-dinitrofluoro- benzene ( DNFB) -induced allergic contact demiatitis (ACD) models with different modeling cycles for the study of skin itch¬ing and inflammation, so as to provide reference and basis for the identification and selection of a more suitable animal model.Methods DNFB was used as a sensitizer, 0.5% DNFB was used to build a 2-week ACD model, and after 5-day sensitiza¬tion, the modeling site was administered once every other day and repeated four times.0.15% DNFB was used to build a 5- week ACD model, and after one week of treatment, DNFB was applied to the modeling site twice a week for four weeks.Behav¬ioral videos were recorded for 60 minutes alter each application of DNFB on the back of the neck for 24 hours.After modeling, Ig-K levels in serum were detected by KLISA, and the skin at the modeling site was stained for histopathology and observed.Results The entire modeling process of both modeled ACD mice was accompanied by severe scratching response after re¬peated skin exposure to DNFB, and the number of scratching significantly increased (P <0.01).Histopathological results showed epidermal thickening ( P < 0.01 ) , hyperkeratosis and inflammatory cell infiltration (P <0.01) in both modeling meth¬ods, and senmi Ig-F levels were significantly elevated ( P < 0.01).Conclusions The contact dennatitis model caused by DNFB is very stable, showing typical pruritus symptoms, severe dermatitis injury and inflammatory immune response, but the 5- week model may have more typical symptoms and allow enough time to observe the effect of the drug, which provides further ex¬perimental basis and evidence for pruritus and inflammation re¬lated drug research.

Animals ; Cyclic GMP ; metabolism ; Ischemic Preconditioning, Myocardial ; Myocytes, Cardiac ; metabolism ; Nitric Oxide ; biosynthesis ; Rats ; Rats, Sprague-Dawley

Biopsy ; Humans ; Kidney ; pathology ; Staining and Labeling ; methods

Adult ; Antibodies, Monoclonal, Murine-Derived ; therapeutic use ; Antigens, CD20 ; metabolism ; Antineoplastic Agents ; therapeutic use ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Cervical Intraepithelial Neoplasia ; drug therapy ; metabolism ; pathology ; surgery ; virology ; Cyclin-Dependent Kinase Inhibitor p16 ; metabolism ; Cyclophosphamide ; therapeutic use ; Doxorubicin ; therapeutic use ; Female ; Follow-Up Studies ; Humans ; Lymphoma, Follicular ; drug therapy ; metabolism ; pathology ; surgery ; virology ; Neoplasm Staging ; Neprilysin ; metabolism ; Papillomavirus Infections ; Prednisone ; therapeutic use ; Receptors, Complement 3d ; metabolism ; Rituximab ; Uterine Cervical Neoplasms ; drug therapy ; metabolism ; pathology ; surgery ; virology ; Vincristine ; therapeutic use

Objective To study the significance of the sample S/Co ratio when using a domestic reagent for anti-hepatitis C virus(HCV)antibody detection and to explore the procedure and standard of anti-HCV antibody diagnosis by using this domestic reagent.Methods Anti-HCV antibody was detected in 295 000 blood donors by a domestic anti-HCV reagent with enzyme-linked immunosorbent assay(ELISA)method and the reactive samples were tested again by ortho anti-HCV antibody reagent.The samples which anti-HCV antibodies were determined as positive by ortho anti-HCV rea- gent were examined by recombinant immunoblot assay(RIBA)reagent and 106 samples of them were also tested for HCV RNA.Results Six hundred and eighty-one samples were reactive in 295 000 samples screened by the domestic ELISA reagent,the reactive ratio was 0.23 %.Among the reactive samples screened by the domestic ELISA reagent,367 samples were determined as positive by ortho anti-HCV reagent while 66.2% of them showed a S/Co ratio≥3.8.The consistency rate between positive results determined by the domestic reagent and RIBA reagent respectively was 53.8%.For the samples showing S/Co ratio≥3.8 by ortho anti-HCV reagent,94.2% had a S/Co ratio≥8.0 when using the domestic ELISA reagent,while the percentage of samples showing S/Co ratio

Alzheimer's Disease (AD) is a chronic neurodegenerative disease that usually takes many years from preclinical phase to prodromal phase characterized by mild symptoms before the onset of dementia. Once diagnosed with AD, the brain is already severely damaged and the disease will process quickly to the most severe stages since there is no medications that reverse the neuronal injuries in the brain. Thus, simple, inexpensive, and widely available methods for detecting potential AD patients during their preclinical phases are urgently needed. In such case, olfactory testing may offer a chance for early diagnosis of AD. However, there are limitations in these olfactory tests due to the complexity of the brain areas it extends to and the frequently olfactory fatigue occurred in the behavioral olfactory tests. Great efforts have been done epidemiologically to investigate the correlation between olfactory functions and possibility of developing AD. Different patterns of olfactory dysfunction have been found in AD at early stages and even mild cognitive impairment (MIC), but the cause of the dysfunction remained unclear. Various kinds of AD animal models have been used in the field to clarify the existence of olfactory dysfunctions and thus study the underling mechanism of the dysfunction. In this review we discuss (1) the function of Tau physiologically and pathologically; (2) the genetic background and biological characteristics of the most commonly used Tau transgenic mice; (3) the structural and molecule basis of olfaction; (4) the possible relationship between Tau pathology and olfactory dysfunction. Finally, we suggest that the tau transgenic mouse models may be helpful in studying the possible mechanisms of the dysfunction.
Alzheimer Disease ; physiopathology ; Animals ; Disease Models, Animal ; Mice ; Mice, Transgenic ; Olfaction Disorders ; physiopathology ; tau Proteins

Objective:to do clinical study on effect of sleep-related behavior modification and relaxation training on insomnia.Method:44 outclinic patients with insomnia received sleep-related behavior modification and relaxation training for 8 weeks. Using self-designed inventory to assess the outcome.Result:the time of sleep increased since the third week, and increased continuously. After the intervention, the rate of satisfaction about sleep increased from 23% at the baseline to 86.1%. 36 of the 44 patients completed the 8-week clinical study. Conclusion:sleep-related behavior modification and relaxation training can improve sleep of patients with insomnia.

Objective:To investigate the effect of astragaloside IV (AS-IV) on the secretion of stromal cell-derived factor-1α (SDF-1α) and CXC chemokine receptor 4 (CXCR4) by high glucose injured human umbilical vein endothelial cells (HUVECs), so as to lay a foundation for further study on AS-IV improving angiogenesis by regulating SDF-1 α/CXCR4 axis of endothelial cells.Methods:HUVECs were isolated and cultured from the umbilical vein of full-term healthy newborns and identified by von Willebrand factor (vWF) combined with 4-diamino-2-phenylindole (DAPI) nuclear staining. The obtained HUVECs was cultured in EGM-2 medium with 30 mmol/L glucose for 120 h to obtain high glucose damaged HUVECs. After intervention with different concentration gradients (25 mg/L, 50 mg/L, 100 mg/L, 200 mg/L, 400 mg/L) AS-IV for 72 hours, the contents of SDF-1α and CXCR4 were detected by enzyme linked immunosorbent assay (ELISA) method to determine the best concentration of AS-IV. The supernatant of damaged HUVECs were collected at 6, 12, 24, 48 and 72 hours after intervention with the best concentration of AS-IV, and the contents of SDF-1α and CXCR4 were detected by ELISA method to determine the best action time of AS-IV. The damaged HUVECs was randomly divided into experimental group and control group, and the blank group was set up at the same time. The experimental group was treated with the best concentration of AS-IV and the best time, the control group and the blank group were treated with the same volume of phosphate buffered saline (PBS) solution, and the contents of SDF-1α and CXCR4 in each group were detected by ELISA method.Results:The vWF factor on the cell membrane was green fluorescence, and the nucleus was blue after DAPI staining. When the fusion image showed green fluorescence, HUVECs were identified by blue fluorescence. The expression of SDF-1α in damaged HUVECs was the best when treated with AS-IV of 100 mg/L for 24 hours (1 642.87 pg/ml), and the expression of CXCR4 in damaged HUVECs was the best when treated with AS-IV of 50 mg/L for 48 hours (8.44 ng/ml). Compared with the control group, the contents of SDF-1α and CXCR4 in the experimental group were significantly increased, and the difference was statistically significant ( P<0.05). While the contents of SDF-1α and CXCR4 in the experiment group were slightly less than those in the blank group and there was no statistically significant difference ( P>0.05). Conclusions:AS-IV can promote the expression of SDF-1α and CXCR4 in HUVECs damaged by high glucose to return to normal physiological level, so as to play the role of vascular repair and neovascularization.

Nicotinic acetylcholine receptors (nAChRs) belong to ligand-gated ion channel receptors, of which α7 nAChR subtype is widely distributed in the cerebral cortex, thalamus, hippocampus, and also identified in microglia, macrophages, bone marrow cells, etc. Previous studies revealed that α7 nAChR is closely related to the function of the cholinergic anti-inflammatory pathway, and is a vital target for drug development of Alzheimer's disease and schizophrenia. The establishment of a stable α7 nAChR in vitro drug screening system is crucial for the efficient screening of novel drugs targeting this target. Recombinant expression of different subtypes of nAChRs on Xenopus laevis oocyte membranes and current detected by two-electrode voltage clamp (TEVC) is an advanced and complex model for novel drug screening. Molecular chaperones can assist the assembly of some nAChR subunits to form functional receptors, providing a stable expression model for the screening of compounds targeting this receptor. In this study, a molecular chaperone gene of α7 nAChR, transmembrane protein 35A (Tmem35a), was isolated and cloned from rats. We constructed the recombinant expression vector and obtained the cRNA of Tmem35a by in vitro transcription technique. Two cRNAs (Tmem35a and α7) were mixed and injected into X. laevis oocytes for expression. Then, the effects of this molecular chaperone on the current expression and pharmacological properties of α7 nAChR were evaluated by the TEVC. The results revealed that TMEM35A, also known as novel acetylcholine receptor chaperone (NACHO) could effectively increase the expression of α7 nAChR protein on oocyte membranes, and the amount of α7 nAChR protein was increased about 1-fold. The peak current induced by agonist acetylcholine (ACh) was increased about 10-fold. After injection of Tmem35a cRNA, the median effect concentration (EC₅₀) value of α7 nAChR to agonist ACh is 228.5 μmol·L^-1, which shows almost no difference from native α7 nAChR (EC₅₀: 223.3 μmol·L^-1), indicating the preservation of the normal properties of α7 nAChR. The results of this investigation indicate that the molecular chaperone NACHO effectively assists the heterologous expression of α7 nAChR in X. laevis oocytes, which provides a model for screening the potency of lead compounds targeting α7 nAChR. All animal experiments in this study were reviewed and approved by the Ethics Committee of Guangxi University (approval number: GXU-2023-0249).