Comparison of Periarticular Injection and Intra-articular Injection for Pain Management After Total Knee Arthroplasty: A Systematic Review and Meta-Analysis.

PURPOSE: Local infiltration analgesia, an essential component of multimodal analgesia after total knee arthroplasty (TKA), can be classified into periarticular injection (PAI) and intra-articular injection (IAI) as per administration techniques. Currently, there is no definite answer of the optimal choice between the two techniques. This meta-analysis aims to determine whether PAI provides superiority of pain relief and functional recovery than IAI after TKA. DESIGN: Systematic review and meta-analysis. METHODS: Comparative studies that compared PAI and IAI in patients after TKA were searched in the Embase, PubMed, MEDLINE, and the Cochrane Library databases. The primary outcomes were visual analog scale scores for pain and opioid consumption. The secondary outcomes were complications, function of recovery, and length of hospital stay. FINDINGS: Four randomized controlled trials and two case-controlled studies with a total of 769 patients were enrolled. There were no significant differences in mean visual analog scale scores at postoperative day 0 (P = .17) and day 1 (P = .27), maximum visual analog scale scores at day 0 (P = .89) and day 1 (P = .82), total opioid consumption at day 1 (P = .96), opioid complications (P = .15), and length of hospital stay (P = .84) between PAI and IAI. CONCLUSIONS: Based on the available evidence, PAI does not offer superior effects at pain control and discharge than IAI after TKA. However, owing to the limited sample size and heterogeneity of the included studies, further large well-designed randomized controlled trials are still needed to validate this conclusion. REGISTRATION: The protocol has been registered in the PROSPERO international database under number CRD42020165138.

Clinical features and outcomes of seven patients with COVID-19 in a family cluster.

BACKGROUND: The family cluster is one of most important modes of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) transmission throughout China, and more details are needed about how family clusters cause the spread of coronavirus disease 2019 (COVID-19). CASE PRESENTATION: We retrospectively reviewed 7 confirmed cases from one family cluster. Both clinical features and laboratory examination results were described. Patient 1 had been in close contact with someone who was later confirmed to have COVID-19 in Wuhan City before he returned back to his hometown. He had dinner with 6 other members in his family. All the persons developed COVID-19 successively except for one older woman who neither had dinner with them nor shared a sleeping room with her husband. Six patients had mild or moderate COVID-19 but one older man with underlying diseases progressed into the severe type. After general and symptomatic treatments, all the patients recovered. CONCLUSIONS: In a family cluster, having dinner together may be an important mode for the transmission of SARS-CoV-2. In this setting, most cases are mild with a favorable prognosis, while elderly patients with underlying diseases may progress into the severe type. For someone who has close contact with a confirmed case, 14-day isolation is necessary to contain virus transmission.

Traffic-related air pollution induces non-allergic eosinophilic airway inflammation and cough hypersensitivity in guinea-pigs.

BACKGROUND: The pathogenesis and pathophysiology of eosinophilia-related chronic cough such as non-asthmatic eosinophilic bronchitis and cough variant asthma are still not clear. OBJECTIVE: This study is to examine the potential role of traffic-related air pollution (TRAP) in eosinophilic inflammation and cough responses. METHODS: Non-sensitized guinea-pigs were exposed to TRAP in an urban traffic tunnel or kept in a filtered air environment for 7 or 14 days. Reflexive cough was measured using citric acid and allyl isothiocyanate (AITC) challenges, respectively. Spontaneous cough counting was determined using audio recording and a waveform analysis. Airway inflammation was evaluated using differential cells in bronchoalveolar lavage fluid (BALF) and lung histopathology. To further elucidate the relationship between airway inflammation and cough hypersensitivity, a subgroup of those exposed for 14 days received a dexamethasone treatment. RESULTS: Compared to reflexive cough count (mean (95% confidence interval) in 10 minutes) provoked by the AITC challenge for the unexposed animals (3.1 (1.7-4.5)), those were increased significantly following both the 7-day (12.0 (6.8-17.2), P < 0.01) and the 14-day (12.0 (6.4-17.6), P < 0.01) TRAP exposure. The effect provoked by the citric acid challenge was more profound following the 14-day exposure (26.0 (19.5-32.5) vs 3.8 (1.5-6.0) for the control, P < 0.001). TRAP exposures enhanced spontaneous cough events, caused a significant increase of eosinophils and neutrophils in BALF and resulted in a dramatic eosinophilic infiltration in submucosal layer of trachea and bronchus, which can be inhibited significantly by dexamethasone treatment. CONCLUSIONS & CLINICAL RELEVANCE: TRAP exposures induced cough hypersensitivity and non-allergic eosinophilic inflammation of airways in guinea-pigs. This study highlights the potential mechanisms of eosinophilia-related chronic cough that can be induced by traffic-related air pollution.

Sodium butyrate alleviates lipopolysaccharide-induced endometritis in mice through inhibiting inflammatory response.

Endometritis is commonly occurred in dairy cows after calving and results in a great deal of property damage. Although numerous studies have been performed to find the therapeutic agents for endometritis, the incidence of this disease remains high. Short-chain fatty acids (SCFAs), the major metabolic products of anaerobic bacteria fermentation in the gut, have been reported to exhibit anti-inflammatory properties. Therefore, the purpose of this study was to investigate the protective effects and mechanisms of sodium butyrate (SB) on lipopolysaccharide (LPS)-induced endometritis in mice. The mice were administered by intraperitoneal injection of SB at 1 h before LPS injection. 24 h later, the uterus tissues were collected. Hematoxylin and eosin (H & E) stained sections of uterus were used to determine the degree of the damage. Uterine myeloperoxidase (MPO) activity was used to analyze neutrophil granulocytes concentration. The levels of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) were measured by ELISA. The activation of the NF-κB signaling pathway proteins were detected by Western blot analysis. The results showed that SB significantly attenuated the pathological injury of the uterus tissues. SB also suppressed LPS-induced MPO activity and the production of inflammatory cytokines TNF-α and IL-1ß. Furthermore, Western blot analysis showed that SB inhibited the activation of NF-κB signaling pathway. In addition, SB could inhibit histone deacetylases. In summary, SB protects against LPS-induced endometritis through HDAC inhibition.

Protective effects of polydatin on LPS-induced endometritis in mice.

Endometritis, a common inflammation of the uterus, often causes severe damage to human and animal reproductive health. Polydatin is a polyphenol extracted from the rhizome of Polygonum cuspidatum that has anti-inflammatory and anti-oxidative effects. The purpose of this study was to investigate the underlying protective effects and mechanisms of polydatin against lipopolysaccharide (LPS)-induced endometritis in mice. The mouse model of endometritis was established by injection of LPS through the vagina. The uterine tissues of each group were gathered to analyze histopathological changes, inflammatory cytokine production, and the degree of activation of the NF-κB and Nrf2 signaling pathways. The myeloperoxidase (MPO) activity assay indicated that polydatin treatment significantly alleviated inflammatory cell infiltration in LPS-induced endometritis mice. Furthermore, polydatin treatment remarkably impeded the expression of TNF-α, IL-1ß, and IL-6 by ELISA assay. Hematoxylin-eosin staining (H&E) showed that polydatin significantly decreased impairment of the uterus. In addition, polydatin was also found to suppress LPS-induced NF-κB activation in a dose-dependent manner. The expression of Nrf2 and HO-1 was enhanced by polydatin treatment. All the results suggest that polydatin helpfully alleviates LPS-induced endometritis by suppressing the NF-ĸB signaling pathway and activating the Nrf2 signaling pathway.

Heterogeneity of cough hypersensitivity mediated by TRPV1 and TRPA1 in patients with chronic refractory cough.

BACKGROUND: The differential sensitivity of cough to antitussive therapies implies the existence of heterogeneity in cough hypersensitivity, but how such heterogeneity is expressed across individual patients is poorly understood. We investigated the phenotypes of cough hypersensitivity by examining transient receptor potential ankyrin 1 (TRPA1)- and transient receptor potential vanilloid 1 (TRPV1)-mediated cough sensitivity in patients with chronic refractory cough. METHODS: Using a selective TRPA1 agonist, allyl isothiocyanate (AITC), we established an AITC cough challenge as a measure of TRPA1-mediated cough sensitivity. The AITC cough challenge and the widely used capsaicin (a selective TRPV1 agonist) cough challenge were performed with 250 patients with chronic refractory cough and 56 healthy subjects. The concentration of AITC or capsaicin solution causing at least two (C2) and five coughs (C5) was recorded. Cough sensitivity was expressed as the mean (95% confidence interval) of log C5, and cough hypersensitivity was defined as a log C5 value lower than that of healthy subjects. RESULTS: A distinct concentration-response effect of inhaled AITC was identified both in patients with chronic refractory cough and in healthy subjects. Cough sensitivity to AITC and capsaicin was significantly higher in patients than in healthy subjects (AITC: 2.42 [2.37-2.48] vs 2.72 [2.66-2.78] mM, p = 0.001; capsaicin: 1.87 [1.75-1.98] vs 2.53 [2.36-2.70] µM, p = 0.001) and was higher in females than in males for both healthy subjects and patients (all p < 0.05). Among the 234 patients who completed both challenges, 25 (10.7%) exhibited hypersensitivity to both AITC and capsaicin, 44 (18.8%) showed hypersensitivity to AITC only, 28 (11.9%) showed hypersensitivity to capsaicin only, and 137 (58.6%) exhibited hypersensitivity to neither. Those with TRPA1- and/or TRPV1-mediated hypersensitivity were predominantly female, while those without TRPA1- and TRPV1-mediated hypersensitivity were mainly male. CONCLUSIONS: Four phenotypes of cough hypersensitivity were identified by the activation of TRPV1 and TRPA1 channels, which supports the existence of heterogeneity in cough pathways and provides a new direction for personalized management of chronic refractory cough. TRIAL REGISTRATION: ClinicalTrials.gov NCT02591550 .

IFN Regulatory Factor 1 Mediates Macrophage Pyroptosis Induced by Oxidized Low-Density Lipoprotein in Patients with Acute Coronary Syndrome.

BACKGROUND: Atherosclerosis (AS) is recognized as a chronic inflammatory disease. It is caused by the interaction between inflammatory cells such as macrophages, dendritic cells, and lipoproteins. Evidence has revealed that macrophage pyroptosis in lesion contributes to the formation of the necrotic core and thinning of the fibrous cap, which plays crucial roles in the onset of acute coronary syndrome (ACS). IFN regulatory factor 1 (IRF-1) is a pleiotropic transcription factor involved in various immune processes and cell death. We propose that IRF-1 may be implicated in macrophage pyroptosis in the pathogenesis of AS and ACS. METHODS: Patients with stable angina, unstable angina, acute myocardial infarction, and clinical presentation of chest pain were enrolled. The expression of IRF-1 in human PBMC-derived macrophages was analyzed. Then, overexpression and inhibition of IRF-1 was performed in macrophages from patients with ACS to explore the possible role and mechanism of IRF-1 involvement in macrophage pyroptosis. RESULTS: The expression of IRF-1 in macrophages was upregulated in ACS patients. The overexpression or inhibition of IRF-1 effectively modulated caspase-1 activation, as well as macrophage lysis, expression of gasdermin D-N (GSDMD-N), production of IL-1ß and IL-18, and activation of NLRP3-ASC inflammasome, which were all inhibited by caspase-1 inhibitor. Further experiments revealed that pyroptosis and the downstream inflammatory response in AS induced by IRF-1 is a process that is dependent on reactive oxygen species (ROS) generation. CONCLUSION: Our observations suggest that IRF-1 potently activates ox-LDL-induced macrophage pyroptosis and may play an important role in AS and ACS.

Statin Attenuated Myocardial Inflammation Induced by PM2.5 in Rats.

BACKGROUND: Here, the study aims to explore the effect of PM2.5 exposure on atherosclerosis in rats. MATERIALS AND METHODS: 32 Wistar rats were selected in our study. An atherosclerosis model was established. All rats were evenly divided into four groups, including normal control group (NC), model control group (MC), model PM2.5 group (PM2.5) and model Atorvastatin group (Atorvastatin). The rats in NC and model control group were treated with saline 1 ml/kg body weight by tail intravenous injection, while the rats in PM2.5 group were exposed to PM2.5 suspension. The rats in atorvastatin group were given atorvastatin by gavage with 10 mg·kg-1·per day for 12 weeks until PM2.5 injection. After 24 h, all rats in each group were sacrificed. Pathological analysis, immunohistochemistry (IHC) and electrophoretic mobility shift assays (EMSA) were carried out. RESULTS: PM2.5 exposure significantly reduced the levels of triglyceride (TG), high density lipoprotein (HDL) and superoxide dismutase (SOD), but promoted the levels of total cholesterol (TC), low density lipoprotein (LDL), atherosclerosis index (AI), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α) and high-sensitivity C-reactive protein (hs-CRP) in the rats of PM2.5 group than MC group (p < 0.05). PM2.5 group showed activated nuclear factor-kappa B (NF-κB), seriously damaged myocardial coronary branches and the highest nuclear translocation rate. Atorvastatin significantly improved the levels of TG, HDL, SOD, interleukin-6 (IL-6), and reduced the levels of TC, LDL, AI, MDA, TNF-α, hs-CRP, oxidized low-density lipoprotein (ox-LDL) and blood pressure, even the nuclear translocation rate. CONCLUSIONS: PM2.5 exposure contributes to atherosclerosis in rats, which correlate with the levels of cholesterol, oxidative stress and inflammatory response. Atorvastatin could attenuate myocardial inflammation caused by PM2.5 exposure in rats.

[Layer-specific Analysis in Patients with ST Segment Elevation Myocardial Infarction].

OBJECTIVES: To evaluate left ventricular wall function after ST segment elevation myocardial infarction(STEMI) by layer-specific analysis and determine if the layer-specific parameters can predict left ventricular remodeling(LVR). METHODS: Thirty nine patients with first STEMI who had successful primary percutaneous coronary intervention(P-PCI) were studied, while 30 healthy individuals were included as normal control. Echocardiographic examinations were performed in STEMI patients within 48 h after P-PCI (before follow-up) and 6 months later (follow-up). Three dimensional cardiac function and longitudinal, circumferential 3-layer strain were analyzed. RESULTS: In STEMI, longitudinal endocardial strain was higher than epicardial strain (P<0.01), circumferential strain decreased from endocardium to epicardium gradually (P<0.01). Longitudinal and circumferential 3-layer strain at follow-up was higher than that before follow-up (P<0.01), but lower than that in control group( P<0.05). LVR group had lower longitudinal and circumferential 3-layer strain (P<0.05). Longitudinal epicardial strain was the independent predictor of LVR(odds ratio:3.332,95% confidence interval:1.124-3.882,P=0.03), the cut off value of -9% yielded 89.5% sensitivity and 70.2% specificity. CONCLUSIONS: Strain decreased from endocardium to epicardium within 48 h after P-PCI in STEMI. Myocardial function was lower in LVR group. Longitudinal epicardial strain could be employed as an independent predictor of LVR after STEMI.

Association between TNF-α gene 308G>A polymorphism and lung cancer risk: a meta-analysis.

Many studies have investigated the association between tumor necrosis factor alpha (TNF-α) gene 308G/A polymorphism and lung cancer risk, but the results were inconsistent. We thus comprehensively searched the PubMed, EMBASE, and BIOSIS Previews databases and extracted data from all eligible articles to estimate the association between TNF-α gene 308G/A polymorphism and lung cancer risk. The pooled odds ratio (OR) with 95 % confidence intervals (CIs) were calculated. Twelve case-control studies in 11 articles involving 2,436 cases and 2,573 controls were included in the meta-analysis to assess the association between TNF-α gene 308G>A polymorphism and susceptibility to lung cancer. Overall, TNF-α gene 308G>A polymorphism was significantly associated with an increased risk of lung cancer for A vs. G (OR = 1.13, 95 % CI 1.00 ~ 1.27, P = 0.04). Subgroup analysis by ethnicity showed that there was a significant association between TNF-α gene 308G>A polymorphism and increased risk of lung cancer in Asians, but not in Caucasians. In subgroup analysis by tumor type, there were significant associations between TNF-α gene 308G>A polymorphism and increased risk of lung cancer in small cell lung cancer (SCLC) for AA+AG vs. GG, in non-small cell lung cancer (NSCLC) for A vs. G, AA vs. GG, and AA+AG vs. GG. No association between the genotypes and different stages of lung cancer was detected. The meta-analysis suggests that TNF-α gene 308G>A polymorphism is associated with an increased risk of lung cancer, particularly among Asians, both for SCLC and NSCLC, considering tumor type.

Left ventricular remodeling and dysfunction in systemic lupus erythematosus: a three-dimensional speckle tracking study.

OBJECTIVE: To analyze left ventricular (LV) global structure and systolic function in patients with systemic lupus erythematosus (SLE) using the three-dimensional (3D) speckle tracking imaging. METHODS: Thirty-four SLE patients and 34 healthy subjects underwent 3D echocardiography to obtain LV ejection fraction (LVEF), sphericity index, 3D LV mass, 3D global longitudinal strain (GLS), global circumferential strain (GCS), global area strain (GAS), and global radial strain (GRS). Disease activity was evaluated for all SLE patients by SLEDAI 2000 (SLEDAI-2K) score. RESULTS: Age, gender, height, weight, diastolic blood pressure, and two-dimensional (2D) LVEF were similar between the 2 groups. Despite no difference was found for sphericity index between the groups, 3D LV mass was increased in SLE patients. All components of strain were significantly reduced in SLE patients. Peak systolic GLS, GCS, GAS, and GRS in SLE patients and controls were -18.2 ± 2.9% versus -21.4 ± 2.5%, -18.4 ± 3.1% versus -20.6 ± 2.5%, -32.2 ± 4.4% versus -36.6 ± 3.4%, and 51.4 ± 10.2% versus 61.9 ± 10.0%, respectively (all P < 0.01). In multivariable regression analysis, SLE was independently associated with GAS (P < 0.001). In SLE patients, peak systolic GLS, GAS, GRS was significantly decreased in those with severe disease activity than among inactivity/mildly activity (all P < 0.05). GLS was independently correlated with SLEDAI score (P = 0.001). CONCLUSION: Three-dimensional speckle tracking imaging is a new simple, rapid method to indentify early abnormalities in SLE patients who may have normal LV systolic function with 2D echocardiography.

[Pathogenesis of plaque destabilization induced by PM2.5 exposure and coping strategies].

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.

The impact of fear of cancer recurrence on the quality of life of breast cancer patients: A longitudinal study of the mediation effect of cortisol and hope.

OBJECTIVE: This longitudinal study sought to explore the impact of cortisol and hope levels on Fear of Cancer Recurrence (FCR) and Quality of Life (QOL) in a cohort of 552 breast cancer patients from three centers in Wuhan City. METHOD: A longitudinal study involving 552 breast cancer patients from three centers in Wuhan City utilized Chinese versions of the Fear of Progression Questionnaire-Short Form (FoP-Q-SF), the Herth Hope Index (HHI), and the Functional Assessment of Cancer Therapy-Breast (FACT-B) scale. Cortisol levels were measured thrice daily, and data was collected longitudinally three times. Data analysis was conducted using SPSS 26.0 and Mplus 8.3, employing a longitudinal path model constructed via the cross-lagged method. RESULTS: The results showed there were significant correlations between FCR, cortisol levels, and QOL at different time points. A significant mediating model was found with outcomes related to hope levels. Specifically, FCR predicted a decrease in hope levels (ß = -0.163, p < 0.001), which in turn led to a decrease in overall QOL (ß = -0.078, p < 0.001), with a mediation effect accounting for 10.34%. Although there were correlations between FCR, cortisol levels, and QOL at different time points, further analysis revealed that cortisol levels did not exhibit a mediating effect between the two (95% confidence interval: -0.002 to 0.001). CONCLUSION: This study demonstrated there were significant correlations among FCR, QOL, and hope levels. Considering hope as a crucial mediator between FCR and QOL, potential intervention strategies for optimizing the QOL of breast cancer patients are proposed.

Profiles of Cough and Associated Risk Factors in Nonhospitalized Individuals With SARS-CoV-2 Omicron Variant Infection: Cross-Sectional Online Survey in China.

BACKGROUND: Cough is a common symptom during and after COVID-19 infection; however, few studies have described the cough profiles of COVID-19. OBJECTIVE: The aim of this study was to investigate the prevalence, severity, and associated risk factors of severe and persistent cough in individuals with COVID-19 during the latest wave of the Omicron variant in China. METHODS: In this nationwide cross-sectional study, we collected information of the characteristics of cough from individuals with infection of the SARS-CoV-2 Omicron variant using an online questionnaire sent between December 31, 2022, and January 11, 2023. RESULTS: There were 11,718 (n=7978, 68.1% female) nonhospitalized responders, with a median age of 37 (IQR 30-47) years who responded at a median of 16 (IQR 12-20) days from infection onset to the time of the survey. Cough was the most common symptom, occurring in 91.7% of participants, followed by fever, fatigue, and nasal congestion (68.8%-87.4%). The median cough visual analog scale (VAS) score was 70 (IQR 50-80) mm. Being female (odds ratio [OR] 1.31, 95% CI 1.20-1.43), having a COVID-19 vaccination history (OR 1.71, 95% CI 1.37-2.12), current smoking (OR 0.48, 95% CI 0.41-0.58), chronic cough (OR 2.04, 95% CI 1.69-2.45), coronary heart disease (OR 1.71, 95% CI 1.17-2.52), asthma (OR 1.22, 95% CI 1.02-1.46), and gastroesophageal reflux disease (GERD) (OR 1.21, 95% CI 1.01-1.45) were independent factors for severe cough (VAS>70, 37.4%). Among all respondents, 35.0% indicated having a productive cough, which was associated with risk factors of being female (OR 1.44, 95% CI 1.31-1.57), having asthma (OR 1.84, 95% CI 1.52-2.22), chronic cough (OR 1.44, 95% CI 1.19-1.74), and GERD (OR 1.22, 95% CI 1.01-1.47). Persistent cough (>3 weeks) occurred in 13.0% of individuals, which was associated with the risk factors of having diabetes (OR 2.24, 95% CI 1.30-3.85), asthma (OR 1.70, 95% CI 1.11-2.62), and chronic cough (OR 1.97, 95% CI 1.32-2.94). CONCLUSIONS: Cough is the most common symptom in nonhospitalized individuals with Omicron SARS-CoV-2 variant infection. Being female, having asthma, chronic cough, GERD, coronary heart disease, diabetes, and a COVID-19 vaccination history emerged as independent factors associated with severe cough, productive cough, and persistent cough.

[Assessment of global left ventricular function in hypertensive patients with normal ventricular geometry using global area strain].

We sought to explore the feasibility of global area strain to assess left ventricular global systolic function in patients with essential hypertension and normal ventricular geometry. Thirty-five essential hypertensive patients with normal ventricular geometry and 30 normally healthy persons as controls were enrolled in this study. The two groups were comparable for age, sex ratio, height, weight, body mass index (BMI), and heart rate. Blood pressures (BPs) were significantly higher in the hypertension group than the control group. Two-dimensional echocardiography and three-dimensional speckle tracking imaging were performed. Left ventricular global area strain (GAS), global longitudinal strain (GLS), global circumferential strain (GCS), global radial strain (GRS), LV volumes, ejection fraction (EF), sphericity index (SPI), left ventricular end-diastolic and end-systolic mass (EDmass and ESmass) and LV mass index (EDmassI and ESmassI) were obtained. Compared with those of the controls, GAS, GLS, GCS, GRS were significantly reduced in hypertensive patients Call P < 0.001). GAS (r = 0.672, P < 0. 001), GLS (r = 0.587, P < 0.001), GCS (r = 0.639, P < 0.001) and GRS (r = 0.685, P < 0.001) were correlated with EF in the pooled population. GAS showed an excellent correlation with GCS (r = 0.905, P < 0.001), GLS (r = 0.892, P < 0.001) and GRS (r = 0.990, P < 0.001). EF measured with 3D-STI was significantly lower in group of hypertension (P < 0.001) than that in the controls. There were no significant differences between the two groups in cardiac output, sphericity index, EDmass and ESmass, LV mass index (EDmassI and ESmassI) calculated with 3D-STI. The study showed that GAS could identify early changes of left ventricular global systolic function in hypertensive patients with normal ventricular geometry.

Atorvastatin ameliorated PM2.5-induced atherosclerosis in rats.

PM2.5 provokes atherosclerotic events. Atorvastatin presents anti-inflammatory and antioxidant activities, and may ameliorate PM2.5-induced atherosclerosis development. The purpose of this study was to investigate the cardiotoxic effect of fine particulate matter (PM2.5) on atherosclerosis (AS) in rats, and the intervention effects of atorvastatin (ATO) on PM2.5-induced AS development. AS model was established using 32 male Wistar rats through intraperitoneal injection of vitamin D3 combined with a high-fat diet (10% fat and 4% cholesterol). The rats were randomly divided into 4 groups: control group, PM2.5-exposed group, ATO group, and ATO treated PM2.5-exposed group. PM2.5 increased levels of TC, TG, LDL, MDA, IL-6, and TNF-α, as well as decreased SOD levels. Besides, PM2.5 also enhanced AI. After the treatment of ATO, most levels of various contents in serum, including TC, TG, LDL, MDA, IL-6, TNF-α, hS-CRP, and ox-LDL, significantly decreased compared to the PM2.5-exposed group. Moreover, after the treatment of ATO, AI was significantly reduced compared to the PM2.5-exposed group. In addition, PM2.5 exacerbated the nuclear translocation and ATO resulted in an obvious decrease in PM2.5-induced nuclear translocation. The present study suggests that PM2.5 could induce oxidative damage and systemic inflammatory response in atherosclerosis model rats, while ATO could ameliorate PM2.5-induced atherosclerosis development, possibly by lowering lipid, inhibiting inflammation, and suppressing oxidation.

Smoking index and COPD duration as potential risk factors for development of osteoporosis in patients with non-small cell lung cancer - A retrospective case control study evaluated by CT Hounsfield unit.

Objective: To investigate the effect of smoking index (calculated as number of cigarettes per day × smoking years) and chronic obstructive pulmonary disease (COPD) duration on osteoporosis (OP)evaluated by opportunistic chest CT in patients with non-small cell lung cancer (NSCLC). Methods: A total of 101 patients diagnosed with NSCLC were included in our cohort study. Among them, 50 patients with a history of smoking and COPD were assigned to the experimental group, while 51 patients without a history of smoking and COPD were assigned to the control group. Hounsfield unit (HU) value was measured by conventional chest CT to investigate the bone mineral density; and the mean values of axial HU value in the upper, middle and lower parts of T4, T7, T10 and L1 vertebral bodies were measured as the study variables. Results: There were no significant differences in gender, age, body mass index, type of lung cancer, clinical stage of lung cancer and comorbidities between the two groups (P = 0.938，P = 0.158，P = 0.722,P = 0.596,P = 0.813,P = 0.655). The overall mean HU values of T4, T7, T10, L1 in the experimental group were 116.60 ± 30.67, 110.56 ± 30.03, 109.18 (96.85-122.95), 94.63 (85.20-104.12) and 106.86 ± 22.26, respectively, which were significantly lower than those in the control group (189.55 ± 34.57, 174.54 ± 35.30, 172.73 (156.33-199.50), 158.20 (141.60-179.40) and 177.50 ± 33.49) (P ＜0.05). And in the experimental group, smoking index and COPD duration were significantly and negatively correlated with HU values (r = -0.627, -0.542, P ＜0.05, respectively). Conclusion: Patients with NSCLC who have a history of smoking and COPD exhibit a notably lower HU value compared to the control groups. Additionally, it has been observed that the smoking index and duration of COPD may be influential factors affecting bone mineral density in NSCLC patients.

Association Between Interleukin-6 Gene Polymorphism and Severity of Coronary Artery Disease in Patients with Diabetes.

Introduction: Previous studies have identified diabetes as a risk factor for coronary heart disease. This study determined the correlation between the IL-6 gene -572 G/C polymorphism and the incidence and severity of coronary heart disease in patients with diabetes. Methods: One hundred four patients with diabetes who were admitted to our hospital from January 2019 to December 2020 were retrospectively enrolled in the current study. These patients were divided into a diabetes only group (group A, 27 patients) and a diabetes complicated by coronary heart disease group (group B, 77 patients). Seventy patients in the latter group were further divided into low, medium, and high Syntax score groups based on coronary angiography results. A correlation analysis between IL-6, blood lipids, and the IL-6 -572 G/C gene levels was performed. Results: The serum IL-6 level in patients with the IL-6-572G/C-GG genotype was higher than patients with the GC and CC genotypes. In patients with diabetes, the presence of the IL-6-572G/C-GG and GC genotypes was associated with a significantly increased risk of developing coronary heart disease. Patients with the IL-6-572G/C-GG genotype and diabetes were shown to have more severe coronary artery lesions compared to patients with the CC genotype. Moreover, the G allele of the IL-6-572G/C gene was linked to a higher risk of coronary heart disease and more severe coronary artery lesions in patients with diabetes compared to the C allele. Conclusion: The IL-6-572G/C gene polymorphism is associated with the incidence and severity of coronary heart disease in patients with diabetes.