Objective To analyze the type and incidence of abnormal chromosome karyotype in peripheral blood of infertile patients with different semen quality.Methods Selectet 292 infertility patients who came to our hospital from January 2018 to December 2021 for G-banding karyotyping and semen analysis.According to the semen analysis results,the patients were divided into abnormal semen quality group and normal control group.We made statistics and analysis on the abnormal karyotypes.Results In the group with abnormal semen quality,20 cases(18.87%)of abnormal karyotypes were found.In the normal control group,9 cases(4.84%)had abnormal karyotypes were found.The comparison of the abnormal rates of peripheral blood chromosome karyotypes between the two groups showed statistical significance(P<0.05).The detection rate of chromosomal abnormalities in patients with Azoospermia was 50%,and sex chromosome abnormalities were the main types of abnormalities in this group.Conclusion Karyotype analysis of infertile patients can effectively analyze the causes of infertility,and has important clinical significance for assisted reproduction and primary prevention of birth defects.

OBJECTIVETo observe the effect of beta(3)-adrenoceptor (AR) in regulating resting intracellular Ca(2+) concentration of the ventricular myocytes and investigate the signaling pathway in rats with experimental heart failure.

METHODSRat models of experimental heart failure were established by ligation of the anterior descending artery, and the myocytes were isolated by enzymatic digestion. The resting intracellular Ca(2+) concentration was determined using laser scanning confocal microscopy (LSCM) in the cells stimulated with 1 micromol/L BRL37344 (a selective beta(3)-AR agonist) alone or in combination with PTX, L-NAME, or methylene blue.

RESULTSIn the ventricular myocytes from normal control rats, BRL373444 reduced the resting intracellular Ca(2+) concentration of by 45.5%, while the reduction increased to 59.4% in the cells from rats with heart failure. In combination with L-NAME (10 micromol/L), methylene blue (10 micromol/L), and PTX (2 microg/ml), BRL373444 caused a reduction in resting intracellular Ca(2+) concentration of the ventricle myocytes from normal control rats by 10.1%, 16.9%, and 15.4%, respectively in control group, while the rate was 16.9%, 19.3%, and 11.7% in the heart failure group.

CONCLUSIONSBeta(3)-AR agonist can decrease the resting intracellular Ca(2+) concentration of the ventricular myocytes, but the reduction is smaller in cells from rats with heart failure than in cells of normal rats. This effect is mediated through the PTX-NOS-NO pathway.

Adrenergic Agonists ; pharmacology ; Adrenergic beta-3 Receptor Agonists ; Animals ; Calcium ; metabolism ; Heart Failure ; chemically induced ; metabolism ; pathology ; Heart Ventricles ; pathology ; In Vitro Techniques ; Intracellular Space ; drug effects ; metabolism ; Male ; Myocytes, Cardiac ; drug effects ; metabolism ; pathology ; Rats ; Rats, Wistar ; Receptors, Adrenergic, beta-3 ; metabolism ; Rest ; Signal Transduction ; drug effects

Photoimmunotherapy (PIT) is an emerging tumor-targeted phototherapy that combines the tumor specificity of monoclonal antibodies with the phototoxicity of light absorbers to rapidly and selectively induce the immunogenic death of target tumor cells. PIT has minimal side effects due to its high specificity. The immunogenic cell death induced by PIT results in rapid maturation of immature dendritic cells proximal to dying tumor cells. Subsequently, the mature dendritic cells present the tumor antigens to CD8+ T cells and induce their activation and proliferation, thus enhancing the antitumor immune response of the host. PIT can also improve the anticancer efficacy by enhancing the penetration of nanomedicines into tumor tissues. In view of the excellent application prospects of PIT, this review summarizes the advances in the immune activation mechanism of PIT, the superenhanced permeability and retention effect, and the new strategies for combinatory therapy, providing references for future research and clinical translation.
Antibodies, Monoclonal/therapeutic use* ; Humans ; Immunotherapy ; Neoplasms/therapy* ; Photosensitizing Agents ; Phototherapy

OBJECTIVE To study the effects of cy cloastragenol （CAG） on carbon tetrachloride （CCl4）-induced hepatic fibrosis（HF）and glycolysis in mice. METHODS Male ICR mice were randomly divided into blank group ，model group ，CAG low-dose，medium-dose and high-dose groups （60，120，240 mg/kg），with 6 mice in each group. Except that blank group was given olive oil intraperitoneally ，the mice in other groups were intraperitoneally injected with 10％CCl4-olive oil solution （5 mL/kg） three times a week for 8 weeks to induce HF model. From the 4th week after modeling ，mice in each drug group were given corresponding drug solution intragastrically （10 mL/kg），and mice in blank group and model group were given 0.5％ sodium carboxymethyl cellulose solution intragastrically （10 mL/kg），once a day for 4 weeks. During the experiment ，the body weight of mice were weighted ；after last gastrogavage ，the liver weight was weighted and liver indexes of mice were calculated. The changes of hepatic injury indexes [aspartate aminotransferase （AST）， alanine aminotransferase （ALT）]， related indexes of HF [hematoxylin-eosin （HE）staining score ，Masson and Picrosirius red staining collagen volume fraction ，collagen Ⅰ，α-smooth muscle actin （α-SMA）] and related indexes of glycolysis [lactic acid （LD），hexokinase（HK），phosphofructokinase（PFK）， pyruvate kinase （PK）] were all detected. RESULTS Compared with model group ，the collagen deposition and fibrosis of mice in each drug group were reduced ，and the body weights of mice （except for CAG low-dose group ）were increased to some extent （P＜0.05）. Liver indexes ，serum levels of ALT and AST ，HE staining score of liver histopathology ，Masson and Picrosirius red staining collagen volume fraction ，protein expression of collagen Ⅰ and α-SMA，serum content of LD ，the levels of HK ，PFK and PK in serum and hepatic tissues （except for hepatic tissue of CAG low-dose group ）were all decreased significantly （P＜0.05）. CONCLUSIONS CAG can improve HF in mice induced by CCl 4，and reduce the levels of key enzymes and products of glycolysis.

Metabolic reprogramming is a common phenomenon in cancer, with aerobic glycolysis being one of its important characteristics. Hypoxia-inducible factor-1α (HIF1Α) is thought to play an important role in aerobic glycolysis. Meanwhile, naringin is a natural flavanone glycoside derived from grapefruits and many other citrus fruits. In this work, we identified glycolytic genes related to HIF1Α by analyzing the colon cancer database. The analysis of extracellular acidification rate and cell function verified the regulatory effects of HIF1Α overexpression on glycolysis, and the proliferation and migration of colon cancer cells. Moreover, naringin was used as an inhibitor of colon cancer cells to illustrate its effect on HIF1Α function. The results showed that the HIF1Α and enolase 2 (ENO2) levels in colon cancer tissues were highly correlated, and their high expression indicated a poor prognosis for colon cancer patients. Mechanistically, HIF1Α directly binds to the DNA promoter region and upregulates the transcription of ENO2; ectopic expression of ENO2 increased aerobic glycolysis in colon cancer cells. Most importantly, we found that the appropriate concentration of naringin inhibited the transcriptional activity of HIF1Α, which in turn decreased aerobic glycolysis in colon cancer cells. Generally, naringin reduces glycolysis in colon cancer cells by reducing the transcriptional activity of HIF1Α and the proliferation and invasion of colon cancer cells. This study helps to elucidate the relationship between colon cancer progression and glucose metabolism, and demonstrates the efficacy of naringin in the treatment of colon cancer.
Glycolysis ; Colonic Neoplasms/metabolism* ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism* ; Phosphopyruvate Hydratase/metabolism* ; Flavanones/pharmacology* ; Cell Line, Tumor ; Databases, Genetic ; Cell Proliferation/drug effects* ; Transfection ; Warburg Effect, Oncologic

Objective: To explore the characteristics of pain sensitivity of autism spectrum disorder (ASD), and to provide reference for clinical comprehensive intervention of ASD. Methods: A case-control study was conducted to investigate the characteristics of pain sensitivity in 142 ASD children and 142 normal children using the items related to pain sensitivity in the Autism Treatment Evaluation Checklist (ATEC). In addition, two recognized ASD model mice (BTBR mice and model mice induced by VPA) were selected as experimental group. The thermal pain threshold and mechanical pain threshold of BTBR mice were measured by electroshock seizure threshold and Von Frey filament test, and the differences of pain characteristics between BTBR mice and control mice were compared, the thermal pain threshold of model mice induced by VPA (VPA rats) was measured by electroshock seizure threshold, and the differences between BTBR mice and control mice (Con) were compared. Results: There was significant difference in pain sensitivity between ASD group and control group (χ 2=0.81，P<0.05), and the sensitivity of ASD children to pain was significantly lower than that of normal control children. The pain sensitivity of BTBR mice and C57BL/6 mice on the 42 nd day after birth was measured. The T-test analysis showed that the time taken for BTBR and C57BL/6 mice to retract their feet on the 42 nd day after birth (3.62±0.38,3.02±0.33)s (t=3.28,P<0.01), and the mechanical pain threshold (9.75±3.58,0.55±0.93)s (t=7.44,P<0.01). The detection of thermal stinging pain in VPA rats and con rats on the 9 th, 11 th, 13 th and 15 th day after birth was detected. The results of t test were as follows:P9(11.34±1.38,9.81±1.64)g, P11(11.37±1.98,9.36±1.11)g, P13(11.53±1.38,9.51±1.01)g and P15(12.05±2.91,8.74±1.60)g (t=-2.79,-2.25,3.95,3.95,P<0.05). Conclusion Compared with normal control children, ASD children show insensitivity to pain which is further supported by two types of animal models for ASD.

Objective To analyze the changing trends of the incidence and onset age of cervical cancer in Jiangsu Province by using cancer registration data from 2009 to 2019. Methods The information of national cancer registries with continuous data from 2009 to 2019 was selected, and the quality control indices of cancer registration must be up to standards. A total of 16 registries were included in this study. Statistical analysis indicators include the crude incidence rate of cervical cancer, age-standardized incidence rate, actual average onset age, age-standardized average onset age, and average annual percentage change (AAPC). A birth cohort model was constructed to analyze the incidence of cervical cancer among women born from 2009 to 2019 and its incidence trend. Results From 2009 to 2019, the crude and age-standardized incidence rates of cervical cancer among women in Jiangsu Province showed upward trends, with AAPCs of 5.62% (95%CI: 3.47−7.82) and 4.14% (95%CI: 2.06−6.27), respectively. The incidence rate of cervical cancer in rural areas (AAPC=4.46, 95%CI: 1.13−7.91) increased more than that in urban areas (AAPC=3.83, 95%CI: 2.81−4.86). The actual average onset age of cervical cancer increased from 51.53 years in 2009 to 55.07 years in 2019 (β=0.36, P<0.05). The age-standardized average onset age increased from 48.89 years in 2009 to 50.43 years in 2019 (β=0.21, P<0.05). The age composition ratios of cervical cancer in the age group of 60 years and older were 31.90% in 2019 and 22.40% in 2009 (β=3.66, P<0.05). The incidence of cervical cancer in the same age group of people with different birth years showed an upward trend with the increase in birth year. Conclusion From 2009 to 2019, the incidence rate of cervical cancer in Jiangsu Province showed an upward trend, and this trend was more obvious in rural areas than in urban areas. In addition, the average onset age of cervical cancer showed an upward trend.

OBJECTIVE To study the inhibitory effects and possible mechanism of naringenin on the activation of hepatic stellate cells. METHODS Using human hepatocytes LO2 as reference， based on drug intervention concentration screened by MTT assay， the effects of naringenin （Western blot assay and trypan blue staining test in 10， 20， 40 μmol/L， immunofluorescence assay in 40 μmol/L） on the expressions of liver fibrosis markers protein （collagen Ⅰ， α-SMA） and mRNA （α1-pro collagen Ⅰ， α-SMA） in human hepatic stellate cells LX2， and the expressions of cell apoptosis and apoptosis-related proteins （Bcl-2， Bax， cleaved caspase-3） were investigated. The apoptosis agents （Z-VAD-FMK， FMK）， ferroptosis pathway inhibitor ferrostatin-1， and programmed death pathway inhibitor necrostatin-1 were used to verify the mechanism of the above effects. RESULTS The naringenin could significantly down-regulate protein expressions of collagen Ⅰ （except for naringenin 10 μmol/L） and α-SMA， mRNA expressions of α1-pro collagen Ⅰ （except for naringenin 10 μmol/L） and α-SMA （P＜0.05）； it also induced LX2 cell apoptosis and increased its apoptotic ratio， down-regulated the protein expression of Bcl-2 while up-regulated the protein expressions of Bax （except for naringenin 10 μmol/L） and cleaved caspase-3 （except for naringenin 10 μmol/L）. FMK could reverse above effects of naringenin on LX2 cells （P＜0.05）. CONCLUSIONS Naringenin can inhibit the activation of hepatic stellate cells LX2 through activating the cell apoptosis signal， which plays ameliorative role in liver fibrosis.

BACKGROUND:Scaffold materials serve as platforms that provide space and structure,playing a crucial role in the regeneration of cartilage tissue.Scholars from around the world are exploring different approaches to fabricate more ideal scaffold materials. OBJECTIVE:To review the design principles and preparation methods of cartilage scaffolds,and to further explore the advantages and limitations of various preparation methods. METHODS:Literature searches were conducted on the databases of CNKI,WanFang Data,PubMed,and FMRS from 1998 to 2023.The search terms were"cartilage repair,cartilage tissue engineering,cartilage scaffold materials,preparation"in Chinese and English.A total of 57 articles were ultimately reviewed. RESULTS AND CONCLUSION:(1)The articular cartilage has a unique structure and limited self-repair capacity after injury.Even if self-repair occurs,the newly formed cartilage is typically fibrocartilage,which is far inferior to normal articular cartilage in terms of structure and mechanical properties.It is difficult to maintain normal function and often leads to degenerative changes.Currently,the design and fabrication of scaffold materials for cartilage repair need to consider the following aspects:biocompatibility and biodegradability,suitable pore structure and porosity,appropriate mechanical properties,and bioactivity.(2)Research on the preparation of cartilage scaffolds has made significant progress,continuously introducing new preparation methods and optimization strategies.These methods have their advantages and disadvantages,providing more possibilities for customized preparation and functional design of cartilage scaffolds according to specific requirements.

BACKGROUND:Bone formation is the process by which osteoblasts synthesize and secrete osteoid and promote its mineralization,which generally involves mechanical signal transduction.Osteoblasts are primarily regulated by mechanical factors such as gravity,compressive stress,tensile stress,fluid shear stress,and hydrostatic pressure in vivo,and different mechanical stimuli modulate the proliferation,differentiation,and apoptosis of osteoblasts through various mechanisms,including hormones,cytoskeletal proteins,and microRNAs.By clarifying the effects of biomechanical forces on osteoblasts,it provides ideas and a reference basis for the treatment of osteometabolic diseases involving osteoblasts. OBJECTIVE:To review the effects of different biomechanical forces on the biological characteristics of osteoblasts. METHODS:We conducted a literature search using PubMed,Web of Science,FMRS,CNKI,and WanFang databases for relevant publications published from 2000 to 2023,covering basic research and tissue engineering studies related to the effects of biomechanical forces on osteoblasts.Ultimately,a total of 70 articles were reviewed. RESULTS AND CONCLUSION:Different biomechanical forces have an impact on the biological characteristics of osteoblasts,including proliferation,differentiation,and apoptosis,and these effects are dependent on the intensity and duration of the applied force.Specifically,the effects are as follows:(1)Under microgravity conditions,osteoblast proliferation and differentiation are inhibited,resulting in a decrease in bone density and the development of osteoporosis.(2)Compared to microgravity,hypergravity has a promoting effect on osteoblast proliferation.(3)The effects of compressive stress on osteoblasts are dependent on the loading intensity and time.Appropriate compressive stress can promote osteoblast proliferation and differentiation,which is beneficial for bone tissue formation and repair,while excessive compressive stress can cause osteoblast apoptosis and bone tissue destruction.(4)The biological effects of different types of tensile stress on osteoblasts differ.Studies have shown that a strain rate within the range of 0-12%has a promoting effect on osteoblast proliferation.(5)Fluid shear stress can promote osteoblast proliferation and differentiation and enhance the bone-inducing effect of biomaterials.(6)Static hydrostatic pressure can affect the biological behavior of osteoblasts,including proliferation,differentiation,and apoptosis,and these effects are closely related to the time and intensity of the pressure.Understanding the effects of different biomechanical forces on osteoblasts is of great significance for a deeper understanding of bone growth and maintenance mechanisms.