Objective: Progressive supranuclear palsy (PSP) involves a variety of visual symptoms that are thought to be partially caused by structural abnormalities of the retina. However, the relationship between retinal structural changes, disease severity, and intracranial alterations remains unknown. We investigated distinct retinal thinning patterns and their relationship with clinical severity and intracranial alterations in a PSP cohort. Methods: We enrolled 19 patients with PSP (38 eyes) and 20 age-matched healthy controls (40 eyes). All of the participants underwent peripapillary and macular optical coherence tomography. Brain 11C-2β-carbomethoxy-3β-(4-fluorophenyl) tropane (11C-CFT) and 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography imaging were also performed in patients with PSP. We investigated the association between retinal thickness changes and clinical features, striatal dopamine transporter availability, and cerebral glucose metabolism. Results: The peripapillary retinal nerve fiber layer (pRNFL) and macula were significantly thinner in patients with PSP than in controls. The thickness of the superior sector of the pRNFL demonstrated a significant negative relationship with the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale part III and Hoehn and Yahr staging scale scores. A significant negative correlation was found between outer inferior macular thickness and disease duration. Outer temporal macular thickness was positively correlated with Montreal Cognitive Assessment scores. In PSP, lower outer temporal macular thickness was also positively correlated with decreased dopamine transporter binding in the caudate. Conclusion The pRNFL and macular thinning may be candidate markers for monitoring disease severity. Additionally, macular thinning may be an in vivo indicator of nigrostriatal dopaminergic cell degeneration in PSP patients.

Objective: To explore the clinical characteristics and prognostic factors of female patients with Stanford type B aortic dissection. Methods: This is a single-centre retrospective study. Consecutive patients diagnosed with Stanford type B aortic dissection in General Hospital of Northern Theater Command from June 2002 to August 2021 were enrolled, and grouped based on sex. According to the general clinical conditions and complications of aortic dissection tear, patients were treated with thoracic endovascular aortic repair, surgery, or optimal medication. The clinical characteristics and aortic imaging data of the patients at different stages were collected, adverse events including all-cause deaths, stroke, and occurrence of aortic-related adverse events were obtained during hospitalization and within 30 days and at 1 and 5 years after discharge. According to the time of death, death was classified as in-hospital death, out-of-hospital death, and in-hospital death was divided into preoperative death, intraoperative death and postoperative death. According to the cause of death, death was classified as aortic death, cardiac death and other causes of death. Aortic-related adverse events within 30 days after discharge included new paraplegia, post-luminal repair syndrome, and aortic death; long-term (≥1 year after discharge) aortic-related adverse events included aortic death, recurrent aortic dissection, endoleak and distal ulcer events. The clinical characteristics, short-term and long-term prognosis was compared between the groups. Logistic regression analysis was used to explore the association between different clinical factors and all-cause mortality within 30 days in female and male groups separately. Results: A total of 1 094 patients with Stanford type B aortic dissection were enrolled, mean age was (53.9±12.1) years, and 861 (78.7%) were male and 233 (21.3%) were female. (1) Clinical characteristics: compared with male patients, female patients were featured with older average age, higher proportion of aged≥60 years old, back pain, anemia, optimal medication treatment, and higher cholesterol level; while lower proportion of smoking and drinking history, body mass index, calcium antagonists use, creatine kinase level, and white blood cell count (all P<0.05). However, there was no significant difference in dissection tear and clinical stage, history of coronary heart disease, diabetes, hypertension, and cerebrovascular disease between female and male patients (all P>0.05). (2) Follow-up result: compared with male patients, female patients had a higher rate of 30-day death [6.9% (16/233) vs. 3.8% (33/861), P=0.047], in-hospital death (5.6% (13/233) vs. 2.7% (23/861), P=0.027), preoperative death (3.9% (9/233) vs. 1.5% (12/861), P=0.023) and aorta death (6.0% (14/233) vs. 3.1% (27/861), P=0.041). The 1-year and 5-year follow-up results demonstrated that there were no significant differences in death, cerebrovascular disease, and aorta-related adverse events between the two groups (all P>0.05). (3) Prognostic factors: the results of the univariate logistic regression analysis showed that body mass index>24 kg/m² (HR=1.087, 95%CI 1.029-1.149, P=0.013), history of anemia (HR=2.987, 95%CI 1.054-8.468, P=0.032), hypertension (HR=1.094, 95%CI 1.047-1.143, P=0.040) and troponin-T>0.05 μg/L (HR=5.818, 95%CI 1.611-21.018, P=0.003)were associated with an increased risk of all-cause mortality within 30 days in female patients. Conclusions: Female patients with Stanford type B aortic dissection have specific clinical characteristics, such as older age at presentation, higher rates of anemia and combined back pain, and higher total cholesterol levels. The risk of death within 1 month is higher in female patients than in male patients, which may be associated with body mass index, hypertension, anemia and troponin-T, but the long-term prognosis for both female and male patients is comparable.
Humans ; Male ; Female ; Adult ; Middle Aged ; Aged ; Prognosis ; Hospital Mortality ; Retrospective Studies ; Troponin T ; Aortic Aneurysm, Thoracic/surgery* ; Blood Vessel Prosthesis Implantation/adverse effects* ; Treatment Outcome ; Endovascular Procedures/adverse effects* ; Aortic Dissection ; Hypertension/complications* ; Cholesterol ; Risk Factors

With the widespread application of extracorporeal membrane oxygenation (ECMO) technology, ECMO centers have been established in most regions of China, and the demand for ECMO transport is also increasing. Critically ill patients with ECMO carry many catheters. ECMO devices and accessories are cumbersome and numerous, requiring a large amount of manpower to assist in the transfer. At present, most of ECMO transport equipment are vertical carts provided by equipment suppliers, which cannot accommodate all ancillary equipment and are difficult to be loaded into ambulances for transportation. Therefore, critically ill patients face many risks if they need to be transported inter-hospital. A specific vehicle for ECMO patients was designed by the medical staff of the department of critical care medicine of Zhujiang Hospital of Southern Medical University, which integrates the ECMO host, oxygenator, centrifugal pump, portable ventilator, coagulation instrument, injection pump, monitor, oxygen cylinder, and etc., to greatly facilitate the transportionation. This invention obtained the National Utility Model Patent of China (ZL 2019 2 1201261.4). The new ECMO transport vehicle can facilitate the interhospital transport of critically ill patients, reduce the occurrence of accidents, shorten the transport time and reduce the number of transport personnel, and has a good clinical application value.

OBJECTIVETo develop a novel colorimetric method for detecting the tumor biomarker vascular endothelial growth factor (VEGF) based on aptamer and magnetic beads.

METHODSThe capture aptamer was hybridized to urease functionalized single-stranded DNA (ssDNA) and immobilize on the surface of magnetic beads by specific biotin-avidin binding. In the presence of VEGF, aptamers bound to VEGF to form a specific stem-loop structure to release the urease functionalized ssDNA. After separation, the supernatant was transferred to a tube and urea and phenol red were added. Urease hydrolyzed urea to produce ammonia to cause an increase of the pH value and a color change of phenol red. The results were inspected with either the naked eyes or by a UV spectrophotometer.

RESULTSUnder optimized conditions, the detection system showed a good linear relationship for VEGF detection in the range of 0.1 to 10 pmol/L with a detection limit as low as 0.06 pmol/L. The results of VEGF detection in the serum of patients with lung cancer were consistent with those using an ELISA Kit. The results of examination of 10 serum samples with this aptamer-based method and ELISA kit showed that the accuracy of this method was 90%.

CONCLUSIONThis aptamer-based system provides an simple and convenient method for VEGF detection with a high sensitivity and selectivity.

With the increasingly more serious environmental pollution in China in recent years, effective intervention with PM25-induced health risks has become a major scientific issue to be addressed urgently in medical research field in China. NOD-like receptors (NLRs) are a family of cytoplasmic pattern-recognition receptors that have critical roles in innate immunity. On the basis of study progresses in international cardiovascular disease research "Fine particulate matter exposure is a modifiable risk factor for the morbidity and mortality of cardiovascular diseases", and with reference to the current understanding of pulmonary inflammation and oxidative stress in PM2.5-induced acute coronary syndrome, this study intended to investigate whether intracellular pattern recognition NL-RP3 plays a important role in the inital event of PM2.5 induced vessel inflammation as a foreign matter in the process of plaque destabilization and to thoroughly explore the underlying mechanisms responsible for PM2.5-induced acute cardiovascular events. On the other hand, it also studies the feasibility of using traditional Chinese medicine to treat plaque destabilization cause by PM2.5 exposure and discuss it's pathogenesis and intervention strategy based on TCM theory. This paper in order to provide scientific basis for social focal issues in public health proactively and offers the references for relevant research.
Air Pollutants ; toxicity ; Animals ; Environmental Exposure ; adverse effects ; Humans ; Medicine, Chinese Traditional ; methods ; Particulate Matter ; toxicity ; Plaque, Atherosclerotic ; chemically induced ; drug therapy ; mortality

This study was purposed to explore the mechanisms of cladribine (2-CdA)-inducing apoptosis of multiple mycloma RPMI 8226 cells. The MTT method was used to determine cell proliferation after being treated with 2-CdA. Apoptosis and cell cycle progression were examined by flow cytometry. Transmission electron microscopy was used to observe ultrastructural changes of RPMI 8226 cells. RT-PCR and Western blot were used to analyze the mRNA and protein expression levels of BCL-2, MCL-2 and caspase-3 respectively. The results showed that the 2-CdA inhibited proliferation of RPMI 8226 cells in time and dose-dependent manner. Typical apoptotic morphological and ultrastructure changes could be observed by electron microscopy. Flow cytometry showed that 2-CdA induced myeloma cell apoptosis and arrested myeloma cells in the G2/M phase. The mRNA expression of BCL-2 and MCL-1 decreased but that of caspase-3 not apparently changed. Western blot results suggested that the change trend of BCL-2 MCL-1 and caspase-3 was the same as result of RT-PCR. It is concluded that 2-CdA exhibits inhibitory effects on RPMI 8226 cells in vitro. Activating the mitochondrial and death receptor pathways of apoptosia may be the potential mechanism, meanwhile, the cell cycle arrest may also play a critical role in apoptosis.
Apoptosis ; drug effects ; Caspase 3 ; Cell Division ; Cell Line, Tumor ; Cell Proliferation ; Cladribine ; pharmacology ; Humans ; Multiple Myeloma ; pathology ; Proto-Oncogene Proteins c-bcl-2

This study was aimed to investigate the effects of mitoxantrone on proliferation and apoptosis of human multiple myeloma cell line RPMI-8226 and its mechanism. The inhibitory rate of RPMI8226 cells proliferation was assayed by MTT, the morphological changes of RPMI-8226 cells were observed by inverted flurescent microscopy and transmission electron microscopy, the apoptosis rate and the cell cycle distribution of RPMI-8226 cells were detected by flow cytometry. The effects of mitoxantrone on the expression of BCL-2, BAX, caspase-3 mRNA were detected by RT-PCR, the BCL-2, BAX, caspase-3 protein expression of RPMI-8226 cells was analyzed by Western blot. The results showed that mitoxantrone could inhibit the proliferation of RPMI-8226 cells in time- and dose-dependent manners. Light microscopy showed that the cell number in mitoxantrone group was significantly less than that in control group and the cell growth arrangement was irregular, apoptotic cells could be seen. Under electron microscope, typical apoptotic morphological and ultrastructural changes could be observed, these results confirmed that the mitoxantrone could induce apoptosis of RPMI-8226 cells, the difference have statistical significance (P < 0.05). The 1.0 µg/ml low concentration of mitoxantrone mainly arrested RPMI-8226 cells in the G2/M phase(P < 0.05), and the 2.0 µg/ml high concentration of mitoxantrone mainly arrested RPMI-8226 cells in the S phase (P < 0.05). The expression of BCL-2 mRNA decreased (P < 0.05),while the expression of BAX, caspase-3 mRNA increased (P < 0.05). Western blot indicated that BCL-2 protein expression also decreased (P < 0.05) and BAX, caspase-3 protein expression increased. It is concluded that the mitoxantrone can inhibit the proliferation of RPMI-8226 cells by inducing cell apoptosis. Activation of the mitochondrial and death receptor pathways of apoptosis may be involved in the mitoxantrone-induced apoptosis, the cell cycle arrest may also play an important role in the apoptosis mechanism.
Apoptosis ; drug effects ; Caspase 3 ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Mitoxantrone ; pharmacology ; Multiple Myeloma ; pathology ; Proto-Oncogene Proteins c-bcl-2

This study was aimed to investigate the effects of sorafenib on proliferation and apoptosis of MM cell line RPMI-8226, and to explore the its potential anti-tumor mechanism. The inhibitory rate of multiple myeloma cell proliferation was tested by MTT. Transmission electron microscopy was used to observe morphological and ultrastructural changes of RPMI-8226 cells treated with sorafenib. The effects of sorafenib on the apoptosis and cell cycle of RPMI-8226 cells was detected by flow cytometry. The effects of sorafenib on the expression of caspase-3, BCL-2 and MCL-1 mRNA and protein were assayed by RT-PCR and Western blot respectively. The results showed that sorafenib (0-10.0 µmol/L) could obviously inhibit the proliferation of RPMI-8226 cells in time and dose-dependent manner. Flow cytometry results showed that sorafenib could induce apoptosis of RPMI-8226 cells, the difference was statistical significance (P < 0.05). Sorafenib mainly arrested RPMI-8226 cells in the G1 phase (P < 0.05). Typical apoptotic morphological and ultrastructural changes of MM cells could be observed under transmission electron microscope, Examination of cellular signaling pathways showed that sorafenib induced upregulation of cleaved-caspase-3 expression, and simultaneous downregulation of BCL-2 and MCL-1 expression. It is concluded that sorafenib displays anti-myeloma activity. Activating the death receptor pathway and arresting cell cycle may be two of the relatated mechanisms.
Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Caspase 3 ; Cell Cycle ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Multiple Myeloma ; drug therapy ; pathology ; Niacinamide ; analogs & derivatives ; pharmacology ; Phenylurea Compounds ; pharmacology ; Proto-Oncogene Proteins c-bcl-2 ; Signal Transduction

This study was aimed to investigate the effects of oxaliplatin on human multiple myeloma cell line RPMI-8226 and its mechanism. The proliferation inhibitory rate of RPMI8226 cells was assayed by MTT, the morphological changes of RPMI-8226 cells were observed by inverted fluorescent microscopy and transmission electron microscopy, the apoptosis rate and the cell cycle distribution of RPMI-8226 cells were detected by flow cytometry, The effects of oxaliplatin on the expression of Bcl-2, caspase-8, caspase-3 mRNA were tested by RT-PCR, Bcl-2 protein expression of RPMI-8226 cells was analyzed by Western blot. The results showed that oxaliplatin could inhibit the proliferation of RPMI-8226 cells in time and dose-dependent manners. Cell number in oxaliplatin group was significantly less than that in control group under light microscope, and the growth arrangement was irregular, apoptotic cells could be seen. Under electron microscope, typical apoptotic morphological and ultrastructural changes could be observed. Flow cytometry results showed that oxaliplatin could induce apoptosis of RPMI-8226 cells, the difference have statistical significance (P < 0.05). Oxaliplatin mainly arrested RPMI-8226 cells in the S phase (P < 0.05). The expression of Bcl-2 mRNA did not have apparent change, while the expression of caspase-8, caspase-3 mRNA increased (P < 0.05). Western blot results suggested that the expression of Bcl-2 protein had no obvious change. It is concluded that the oxaliplatin can induce apoptosis of RPMI-8226 cells, activating the death receptor pathway and arresting cell cycle may be two of the related mechanisms, Bcl-2 gene has unobservable effects in the process of oxaliplatin-induced cell apoptosis.
Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Caspase 8 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Multiple Myeloma ; metabolism ; pathology ; Organoplatinum Compounds ; pharmacology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism

This study was aimed to investigate the effects of docetaxel on proliferation and apoptosis of multiple myeloma cell line RPMI8226 and its mechanism. The inhibitory rate of multiple myeloma cells was detected by MTT, the morphological and ultrastructural changes of RPMI8226 cells were observed by using inverted fluorescent microscope and transmission electron microscope, the apoptosis-inducing effect of docetaxel on RPMI-8226 cells was determined by flow cytometry with Annexin-V FITC/PI staining, the cell distribution in cell cycle of RPMI-8226 cells was assayed using flow cytometry with PI staining; the effect of docetaxel on expression of BCL-2, caspase-8, caspase-3 mRNA was detected by semiquantitative RT-PCR, the expression changes of BCL-2 protein in RPMI-8226 cells before and after treatment with docetaxel were measured by using Western blot. The results indicated that 0.25 - 8.0 µg/ml docetaxel obviously inhibited the proliferation of RPMI-8226 cells in both time- and dose-dependent manners. Cell number of docetaxel-treated group was significantly less than control group under inverted fluorescent microscope, and the cell arrangement was irregular, necrotic cells could be seen occasionally. By transmission electron microscope, the morphological and ultrastructural changes of cell typical apoptosis could be observed, a few necrotic cells could be captured, too. Compared with control group, docetaxel induced the apoptosis of RPMI-8226 cell line (P < 0.01). Docetaxel mainly arrested RPMI-8226 cells in the G(2)/M phase (P < 0.01). The expression of BCL-2 mRNA decreased (P < 0.05), while the mRNA expression of caspase-8 and caspase-3 increased (P < 0.05). Western blot indicated that BCL-2 protein expression also decreased (P < 0.05). It is concluded that docetaxel can inhibit the proliferation of RPMI-8226 cells by inducing cell apoptosis. Activation of the mitochondrial and death receptor pathways of apoptosis may be involved in the docetaxel-induced apoptosis, cell cycle arrest may also play an important role in the apoptosis mechanism.
Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Caspase 8 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Multiple Myeloma ; metabolism ; pathology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Taxoids ; pharmacology