Aldehyde dehydrogenase 2 rs671 a/A Genotype is Associated with an Increased Risk of Early Onset Coronary Artery Stenosis.

Background: The role of aldehyde dehydrogenase 2 (ALDH2) in cardiovascular diseases has been gradually studied. However, it is unclear whether ALDH2 polymorphism is associated with the risk of early onset (onset age ≤55 years old in men and ≤65 years old in women) coronary artery stenosis (CAS). The association between ALDH2 single nucleotide polymorphism (SNP) rs671 and risk in patients with early onset CAS was investigated in this study. Methods: The study included 213 early onset CAS patients and 352 individuals without CAS were set as controls. The ALDH2 rs671 polymorphism was genotyped by polymerase chain reaction (PCR) - microarray. Differences in ALDH2 rs671 genotypes and alleles between patients and controls were compared. Multiple logistic regression analysis was performed after adjusting for gender, body mass index (BMI), smoking history, drinking history, and diabetes mellitus to assess the relationship between ALDH2 rs671 genotypes and early onset CAS risk. Results: The frequency of the ALDH2 rs671 G/G genotype was lower in the early onset CAS patients (43.7% vs 55.3%, p=0.007) than that in the controls. The frequency of the ALDH2 rs671 A allele was higher (32.9% vs 25.0%) than that in the controls (p=0.005). After adjusting for other confounding factors, multivariate logistic regression showed that ALDH2 rs671 A/A genotype (A/A vs G/G: odds ratio (OR) 2.508, 95% confidence interval (CI): 1.130-5.569, p=0.024), overweight (BMI≥24.0 vs 18.5-23.9: OR 5.047, 95% CI: 3.275-7.777, p<0.001), history of smoking (yes vs no: OR 2.813, 95% CI: 1.595-4.961, p<0.001), and diabetes mellitus (yes vs no: OR 2.191, 95% CI: 1.397-3.437, p=0.001) were the independent risk factors of early onset CAS. Conclusion: In men ≤55 years old and women ≤65 years old, individuals with ALDH2 rs671 A/A genotype, overweight (BMI ≥24.0 kg/m2), smoking history, and diabetes mellitus increased risk of developing CAS.

Recent Advancement in Inhaled Nano-drug Delivery for Pulmonary, Nasal, and Nose-to-brain Diseases.

Pulmonary, nasal, and nose-to-brain diseases involve clinical approaches, such as bronchodilators, inhaled steroids, oxygen therapy, antibiotics, antihistamines, nasal steroids, decongestants, intranasal drug delivery, neurostimulation, and surgery to treat patients. However, systemic medicines have serious adverse effects, necessitating the development of inhaled formulations that allow precise drug delivery to the airways with minimum systemic drug exposure. Particle size, surface charge, biocompatibility, drug capacity, and mucoadhesive are unique chemical and physical features that must be considered for pulmonary and nasal delivery routes due to anatomical and permeability considerations. The traditional management of numerous chronic diseases has a variety of drawbacks. As a result, targeted medicine delivery systems that employ nanotechnology enhancer drug efficiency and optimize the overall outcome are created. The pulmonary route is one of the most essential targeted drug delivery systems because it allows the administering of drugs locally and systemically to the lungs, nasal cavity, and brain. Furthermore, the lungs' beneficial characteristics, such as their ability to inhibit first-pass metabolism and their thin epithelial layer, help treat several health complications. The potential to serve as noninvasive self-administration delivery sites of the lung and nasal routes is discussed in this script. New methods for treating respiratory and some systemic diseases with inhalation have been explored and highlight particular attention to using specialized nanocarriers for delivering various drugs via the nasal and pulmonary pathways. The design and development of inhaled nanomedicine for pulmonary, nasal, and respiratory medicine applications is a potential approach for clinical translation.

T2 mapping and readout segmentation of long variable echo-train diffusion-weighted imaging for the differentiation of parotid gland tumors.

OBJECTIVE: To investigate the diagnostic value of radial turbo-spin-echo (TSE) T2 mapping and readout segmentation of long variable echo-train diffusion-weighted imaging (RESOLVE DWI) for the differentiation of parotid gland tumors. MATERIALS AND METHODS: One hundred and fifty-four patients with histopathologically confirmed parotid gland tumors were retrospectively recruited from June 2018 to May 2021 at the First Affiliated Hospital of Zhengzhou University. There were 111 benign tumors and 43 malignant tumors. Benign tumors were further divided into pleomorphic adenomas (n = 69) and Warthin's tumors (n = 26). All patients were scanned using T2 mapping and RESOLVE DWI. T2 and ADC values and a combination of the two methods were compared and analyzed for the ability to differentiate parotid gland tumor types. RESULTS: The T2 and ADC values of benign tumors were significantly higher than those of the malignant tumors (127.97 ± 56.29 ms vs 97.53 ± 45.24 ms, 1.27 ± 0.40 × 10-3 mm2/s vs 1.00 ± 0.39 × 10-3 mm2/s, all P < 0.05). The area under the curve (AUC) of the T2 and ADC values for differentiating (1) benign and malignant parotid tumors, (2) pleomorphic adenomas and Warthin's tumors, (3) pleomorphic adenomas and malignant tumors, and (4) Warthin's tumors and malignant tumors were 0.709 and 0.715, 0.918 and 0.994, 0.748 and 0.774, and 0.665 and 0.659, respectively, with no significant differences observed between the T2 and ADC values (all P > 0.05). There were no significant differences in these values among the three tumor groups (malignant tumor, pleomorphic adenoma, and Warthin's tumor groups, all P > 0.05). CONCLUSIONS: T2 mapping and RESOLVE DWI can be used to differentiate various parotid gland tumors. T2 values are comparable to ADC values.

Elevated Serum Human Epididymis Protein 4 Is Associated With Disease Activity and Systemic Involvements in Primary Sjögren's Syndrome.

Background: We aimed to investigate the clinical utility of human epididymis protein 4, a tumor biomarker being widely utilized in clinical practice in the diagnosis of ovarian cancer, in primary Sjögren's Syndrome (pSS). Methods: A total of 109 pSS patients and 113 healthy controls (HCs) were included in the study. HE4 were determined by Roche Cobas E601 electrochemical luminescence analyzer. Clinical and laboratory findings were reviewed, and the relationships between HE4 and clinical parameters were determined by Spearman's correlation test. The European league against rheumatism Sjögren's syndrome disease activity index (ESSDAI) was utilized to evaluate disease activity. Findings: The levels of HE4 were significantly elevated in patients with pSS compared to HCs (103.65 pmol/L vs. 46.52 pmol/L, p<0.001). The levels of HE4 were positively correlated with ESSDAI scores (r=0.462, p<0.001). Significant positive correlations between the levels of HE4 with pulmonary involvements (r=0.442, p<0.001) and renal involvements (r=0.320, p=0.001) were observed. Receiver operating curve (ROC) analysis revealed an optimal cut-off value of 104.90 pmol/L and 128.05 pmol/L for distinguishing patients with pulmonary and renal involvements, with the areas under the ROC curve (AUCs) of 0.778 (95%CI 0.685-0.870, p<0.001) and 0.768 (95%CI 0.646-0.891, p=0.001), respectively. Among patients with pulmonary involvement, the levels of HE4 were positively correlated with the semiquantitative HRCT grade (r=0.417, p=0.016), and negatively correlated with the percentage of forced vital capacity (FVC) (r= -0.460, p=0.047) and diffusing capacity of the lung for carbon monoxide (DLco) (r= -0.623, p=0.004). For patients with renal involvement, HE4 was positively correlated with creatinine (r=0.588, p=0.021) and negatively correlated with estimated glomerular filtration rate (r= -0.599, p=0.030). Conclusions: Our findings demonstrated a novel role of HE4 in clinical stratification of pSS, suggesting that introducing HE4 to the current pSS test panel may provide additional diagnostic value, particularly in evaluating disease activity and pulmonary/renal involvements.

Granulomatous orchitis: case report and review of the literature.

We report the disease characteristics, diagnosis, and treatment of granulomatous orchitis. A 38-year-old man presented with a history of intermittent swelling, pain, and discomfort in the right testicle of 3 days' duration. Unenhanced magnetic resonance imaging (MRI) of the testis and scrotum revealed an oval mass in the right testis measuring approximately 17 mm in diameter, with clear borders and a target ring-like appearance from periphery to center. T1-weighted imaging (T1WI) showed uniform low-intensity signals, and T2WI showed mixed high- and low-intensity signals. Diffusion-weighted imaging (DWI) signals were iso-intense, and the outer ring on enhanced scans showed progressive enhancement. We performed radical resection of the right testis under combined spinal-epidural anesthesia. The pathological diagnosis was granulomatous right orchitis. Two months postoperatively, ultrasonography showed no testis and epididymal echo signals in the right scrotum, and no obvious abnormalities; color Doppler blood flow imaging (CDFI) findings were normal. Granulomatous orchitis is rare in clinical practice, and the cause is unknown. The disease involves non-specific inflammation; however, it is currently believed that antibiotics and steroids are ineffective for conservative treatment, and orchiectomy should be actively performed.

Exploiting bacterial outer membrane vesicles as a cross-protective vaccine candidate against avian pathogenic Escherichia coli (APEC).

BACKGROUND: The well-known fact that avian pathogenic Escherichia coli (APEC) is harder to prevent due to its numerous serogroups has promoted the development of biological immunostimulatory materials as new vaccine candidates in poultry farms. Bacterial outer membrane vesicles (OMVs), known as spherical nanovesicles enriched with various immunostimulants, are naturally secreted by Gram-negative bacteria, and have gained much attention for developing effective vaccine candidates. Recent report has demonstrated that OMVs of APEC O78 can induce protective immunity in chickens. Here, a novel multi-serogroup OMVs (MOMVs) vaccine was developed to achieve cross-protection against APEC infection in broiler chickens. RESULTS: In this study, OMVs produced by three APEC strains were isolated, purified and prepared into MOMVs by mixing these three OMVs. By using SDS-PAGE and LC-MS/MS, 159 proteins were identified in MOMVs and the subcellular location and biological functions of 20 most abundant proteins were analyzed. The immunogenicity of MOMVs was evaluated, and the results showed that MOMVs could elicit innate immune responses, including internalization by chicken macrophage and production of immunomodulatory cytokines. Vaccination with MOMVs induced specific broad-spectrum antibodies as well as Th1 and Th17 immune responses. The animal experiment has confirmed that immunization with an appropriate dose of MOMVs could not cause any adverse effect and was able to reduce bacteria loads and pro-inflammatory cytokines production, thus providing effective cross-protection against lethal infections induced by multi-serogroup APEC strains in chickens. Further experiments indicated that, although vesicular proteins were able to induce stronger protective efficiency than lipopolysaccharide, both vesicular proteins and lipopolysaccharide are crucial in MOMVs-mediated protection. CONCLUSIONS: The multi-serogroup nanovesicles produced by APEC strains will open up a new way for the development of next generation vaccines with low toxicity and broad protection in the treatment and control of APEC infection.

Programming changes in GLUT1 mediated the accumulation of AGEs and matrix degradation in the articular cartilage of female adult rats after prenatal caffeine exposure.

Osteoarthritis is associated with intrauterine growth retardation (IUGR) and abnormal glucose metabolism. Our laboratory previously reported that prenatal caffeine exposure (PCE) can induce intrauterine maternal glucocorticoid (GC) overexposure in IUGR offspring and increase susceptibility to osteoarthritis after birth. In the present study, we demonstrated the essential role of glucose transporter 1 (GLUT1) programming changes in the increased matrix degradation of articular cartilage and susceptibility to osteoarthritis in female PCE adult offspring. In vivo, we found that PCE decreased the matrix content but did not significantly change the expression of matrix degradation-related genes in the articular cartilage of female fetal rats. The decreased expression of IGF1 and GLUT1 and the content of advanced-glycation-end-products (AGEs) were also detected. At different postnatal stages (2, 6, and 12 weeks), the cartilage matrix content decreased while the degradation-related genes expression increased in the PCE group. Meanwhile, the expression of IGF1 and GLUT1 and AGEs content in the local cartilage increased. In vitro, the expression levels of IGF1 and GLUT1 were inhibited by corticosterone but remained unchanged under caffeine treatment. Exogenous IGF1 can reverse the corticosterone-induced decrease in GLUT1 expression and promote AGEs production, while mifepristone (a glucocorticoid receptor inhibitor) reversed the corticosterone-induced low expression of IGF1 and GLUT1. Exogenous AGEs can increase the expression of inflammatory factors (IL-6 and TNF-α) and degradation-related genes, and decrease the matrix synthesis-related genes expression in chondrocyte. In conclusion, the GC-IGF1-GLUT1 axis mediated intrauterine dysplasia of articular cartilage, increased accumulation of AGEs and matrix degradation after birth in PCE female offspring, thereby increasing their susceptibility to osteoarthritis in adulthood.

A Nanobody Against Cytotoxic T-Lymphocyte Associated Antigen-4 Increases the Anti-Tumor Effects of Specific CD8+ T Cells.

Adoptive cell-based immunotherapy typically utilizes cytotoxic T lymphocytes (CTLs), expanding these cells ex vivo. Such expansion is traditionally accomplished through the use of autologous APCs that are capable of interactions with T cells. However, incidental inhibitory program such as CTLA-4 pathway can impair T cell proliferation. We therefore designed a nanobody which is specific for CTLA-4 (CTLA-4 Nb 16), and we then used this molecule to assess its ability to disrupt CTLA-4 signaling and thereby overcome negative costimulation of T cells. With CTLA-4 Nb16 stimulation, dendritic cell/hepatocellular carcinoma fusion cells (DC/HepG2-FCs) enhanced autologous CD8+ T cell proliferation and production of IFN-γ in vitro, thereby leading to enhanced killing of tumor cells. Using this approach in the context of adoptive CD8+ immunotherapy led to a marked suppression of tumor growth in murine NOD/SCID hepatocarcinoma or breast cancer xenograft models. We also observed significantly increased tumor cell apoptosis, and corresponding increases in murine survival. These findings thus demonstrate that in response to nanobody stimulation, DC/tumor cells-FC-induced specific CTLs exhibit superior anti-tumor efficacy, making this a potentially valuable means of achieving better adoptive immunotherapy outcomes in cancer patients.

High-throughput lipidomics reveal mirabilite regulating lipid metabolism as anticancer therapeutics.

Altered lipid metabolism is an emerging hallmark of cancers. Mirabilite has a therapeutic effect on colorectal cancer (CRC); however, its metabolic mechanism remains unclear. This study aims to explore the potential therapeutic targets of mirabilite protection against colorectal cancer in APCmin/+ mice model. Oral administration of mirabilite was started from the ninth month, while the same dosage of distilled water was given to both the control group and the model group. Based on lipidomics, we collected serum samples of all mice at the 20th week and used a non-targeted method to identify the lipid biomarkers of CRC. Compared with C57BL/6J mice, the metabolic profile of CRC model mice was significantly disturbed, and we identified that 25 lipid-related biomarkers, including linoleic acid, 2-hydroxybutyric acid, 6-deoxocastasterone, hypoxanthine, PC(16:1), PC(18:4), and retinyl acetate, were associated with CRC. According to the abovementioned results, there were six lipid molecules with significant differences that can be used as new targets for handling of CRC through six metabolic pathways, namely, linoleic acid metabolism, retinol metabolism, propanoate metabolism, arachidonic acid metabolism, biosynthesis of unsaturated fatty acids and purine metabolism. Compared with the model group, the metabolic profiles of these disorders tend to recover after treatment. These results indicated that the lipid molecules associated with CRC were regulated by mirabilite. In addition, we identified seven key lipid molecules, of which four had statistical significance. After administration of mirabilite, all disordered metabolic pathways showed different degrees of regulation. In conclusion, high-throughput lipidomics approach revealed mirabilite regulating the altered lipid metabolism as anticancer therapeutics.

Targeting of AUF1 to vascular endothelial cells as a novel anti-aging therapy.

BACKGROUND: Inhibition of aging of vascular endothelial cells (VECs) may delay aging and prolong life. The goal of this study was to prepare anti-CD31 monoclonal antibody conjugated PEG-modified liposomes containing the AU-rich region connecting factor 1 (AUF1) gene (CD31-PILs-AUF1) and to explore the effects of targeting CD31-PILs-AUF1 to aging VECs. METHODS: The mean particle sizes of various PEGylated immunoliposomes (PILs) were measured using a Zetasizer Nano ZS. Gel retardation assay was used to confirm whether PILs had encapsulated the AUF1 plasmid successfully. Fluorescence microscopy and flow cytometry were used to quantify binding of CD31-PILs-AUF1 to target cells. Flow cytometry was also used to analyze the cell cycles of aging bEnd3 cells treated with CD31-PILs-AUF1. We also developed an aging mouse model by treating mice with D-galactose. Enzyme-linked immunosorbent assay (ELISA) was used to evaluate the levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). The malondialdehyde (MDA) and the superoxide dismutase (SOD) levels were detected by commercial kits. Hematoxylin-eosin (HE) staining was used to determine whether treatment with CD31-PILs-AUF1 was toxic to the mice. RESULTS: CD31-PILs-AUF1 specifically could targeted bEnd3 VECs and increased the percentage of cells in the S and G2/M phases of aging bEnd3 cells. ELISA showed that content of the IL-6 and TNF-α decreased in CD31-PILs-AUF1 group. The level of SOD increased, whereas MDA decreased in the CD31-PILs-AUF1 group. Additionally, CD31-PILs-AUF1 was not toxic to the mice. CONCLUSION: CD31-PILs-AUF1 targets VECs and may delay their senescence.

MicroRNA-497 suppresses renal cell carcinoma by targeting VEGFR-2 in ACHN cells.

Abnormal expression of miRNAs contributed to cancers through regulation of proliferation, apoptosis and drug resistance of cancer cells. The present study was designed to investigate the effect of miR-497 on renal cell carcinoma (RCC) and its possible mechanism. Forty paired clear cell RCC (ccRCC) tissues and adjacent normal kidney tissues were obtained from patients, who were not treated by chemotherapy or radiotherapy. RT-PCR was performed to detect expression of miR-497 in the ccRCC tissues. Effects of miR-497 on cell viability, apoptosis, migration and invasion were detected in ACHN cells. Western blotting (WB) was employed to detect the downstream targets of miR-497 We found that miR-497 in ccRCC tissues was decreased. We treated ACHN cells with miR-497 mimics and inhibitors in vitro and found that miR-497 inhibited viability, migration and invasion of ACHN cells. miR-497 promoted ACHN cells' apoptosis. VEGFR-2 was predicted as a possible target of miR-497 Luciferase reporter assay proved that miR-497 suppressed VEGFR-2 directly by binding to its 3'-UTR. Further studies showed that miR-497 influenced the MEK/ERK and p38 MAPK signalling pathways. Our findings demonstrated that miR-497 could suppress RCC by targeting VEGFR-2.

miRNA-34b is directly involved in the aging of macrophages.

BACKGROUND: MicroRNAs (miRNAs) are a class of short noncoding RNA that play important regulatory roles in living organisms. These RNA molecules are implicated in the development and progression of malignant diseases such as cancer and are closely associated with cell aging. Findings demonstrating that microRNA is associated with aging in macrophages have nevertheless rarely been reported. AIMS: This study's objective was to investigate if miRNA-34 is linked to aging process of macrophages. METHODS: We built a cell aging model in mouse RAW264.7 macrophages using D-galactose and determined the expression levels of miRNA-34a, miRNA-34b, and miRNA-34c in aging and normal macrophages by fluorescence quantitative polymerase chain reaction (q-PCR). We predicted a target gene of miRNA-34 using biological information techniques and constructed the recombinant plasmid pGL3-E2f3 for the putative target gene E2f3. RESULTS: The expression level of miRNA-34b was 5.23 times higher in aging macrophages than in normal macrophages. The luciferase activity decreased by nearly 50 % in cells transfected with miRNA-34b mimics, while no significant decrease in luciferase activity was noted in cells transfected with the miRNA-34b inhibitor or unrelated sequences. DISCUSSION: Our findings provide the groundwork for further research into the molecular mechanisms whereby miRNA-34b regulates the aging of macrophages. CONCLUSIONS: miRNA-34b is associated with the aging of RAW264.7 macrophages, and E2f3 is a target gene of miRNA-34b.

The birth of a giant panda: Tracking the biological factors that successfully contribute to conception through to postnatal development.

Reproducing giant pandas (Ailuropoda melanoleuca) remains the most challenging aspect of managed care of this species. However, advancement in knowledge stemming from basic science research on the giant panda has facilitated a growth in the population. Here, we report the successful application of reproductive technologies, including noninvasive hormone monitoring, behavioral/morphometric observations, ultrasonographic evaluations, and acute phase protein assessment, in an individual female. By applying these approaches to one female, we report the practicality and usefulness of a multidisciplinary approach to reproductive care of the species. In addition, the utilization of various technologies across multiple physiological states also provided us an opportunity to record previously understudied events, such as maternal response to weaning and growth of a conceptus.

Effectiveness of Panax ginseng on Acute Myocardial Ischemia Reperfusion Injury Was Abolished by Flutamide via Endogenous Testosterone-Mediated Akt Pathway.

Mechanisms for Panax ginseng's cardioprotective effect against ischemia reperfusion injury involve the estrogen-mediated pathway, but little is known about the role of androgen. A standardized Panax ginseng extract (RSE) was orally given with or without flutamide in a left anterior descending coronary artery ligation rat model. Infarct size, CK and LDH activities were measured. Time-related changes of NO, PI3K/Akt/eNOS signaling, and testosterone concentration were also investigated. RSE (80 mg/kg) significantly inhibited myocardial infarction and CK and LDH activities, while coadministration of flutamide abolished this effect of RSE. NO was increased by RSE and reached a peak after 15 min of ischemia; however, flutamide cotreatment suppressed this elevation. Western blot analysis showed that RSE significantly reversed the decreases of expression and activation of PI3K, Akt, and eNOS evoked by ischemia, whereas flutamide attenuated the effects of these protective mechanisms induced by RSE. RSE completely reversed the dropping of endogenous testosterone level induced by I/R injury. Flutamide plus RSE treatment not only abolished RSE's effect but also produced a dramatic change on endogenous testosterone level after pretreatment and ischemia. Our results for the first time indicate that blocking androgen receptor abolishes the ability of Panax ginseng to protect the heart from myocardial I/R injury.

Impact of smoking and smoking cessation on arterial stiffness in healthy participants.

Smoking is associated with increased arterial stiffness. However, the impact of smoking cessation on arterial stiffness remains unknown. We investigated the effect of smoking cessation on arterial stiffness. Healthy participants (n = 209) were divided into nonsmoking (NSm, n = 96), quit smoking (QSm, n = 61), and maintained smoking groups (MSm, n = 52). Arterial stiffness indexes (ankle-brachial index [ABI] and brachial-ankle pulse wave velocity [baPWV]) were assessed at baseline, and after 6 and 12 months. Baseline, arterial stiffness was significantly higher in the MSm and QSm groups than in the NSm group (P < .001). In the QSm group, there was significant difference in ABI between baseline and 12 months (P = .03). No significant differences were shown in baPWV. Both ABI and baPWV were similar between QSm and MSm group at 12 months. However, there was significant difference between QSm and NSm groups (P < .001). This study shows that 12 months of smoking cessation is associated with improved arterial stiffness.

miR-200c inhibits invasion and migration in human colon cancer cells SW480/620 by targeting ZEB1.

MicroRNAs are a class of ≈22-nt noncoding single-strand RNAs regulating gene expression postscriptionally. Metastasis caused poor prognosis in colorectal cancer patients and half of the patients developed metastatic lesions when admission. Here we investigated the possible roles of microRNAs in regulating metastasis in the paired colon cancer cells SW480 and SW620. Among those dysregulated microRNAs, miR-200c was speculated to inhibit metastasis by targeting ZEB1. Overexpression of miR-200c was concurrent with downregulation of ZEB1 mRNA and protein. Functional assays demonstrated that modulation of miR-200c with mimics or inhibitors changed potential of metastasis in SW480/620 cancer cells in vitro. Taken together, our study demonstrated that miR-200c inhibits metastatic ability by targeting ZEB1 in colon cancer cells SW480/620 and suggested that modulation of miR-200c could serve as therapeutic tool for inhibiting metastasis in colorectal cancer.

Localized expression of human BMP-7 by BM-MSCs enhances renal repair in an in vivo model of ischemia-reperfusion injury.

Ischemia and subsequent reperfusion (I/R) damage kidney tubular cells and consequently impair renal function. Rabbit bone marrow mesenchymal stem cells (BM-MSCs) expressing human bone morphogenic protein-7 (hBMP-7) regenerated tubular cells and improved renal function in a kidney I/R model. Rabbits were injected immediately after I/R with one of the following: (i) hBMP-7-transduced BM-MSCs (BM-MSCshBMP-7); (ii) enhanced green fluorescent protein-transduced BM-MSCs (BM-MSCsEGFP); or (iii) PBS. The activity of superoxide dismutase (SOD) was higher, and the amount of malondialdehyde (MDA) was lower in the BM-MSCshBMP-7 group than in the BM-MSCsEGFP group. Both the BM-MSCshBMP-7 group and the BM-MSCsEGFP group had higher SOD activity and lower amounts of MDA than the PBS group. Bcl-2- and Bcl-2-associated X protein levels, and other variables, indicated the regeneration of the kidney in both experimental groups. However, the BM-MSCs (hBMP-7) group showed higher activity than the BM-MSCsEGFP group, indicating that the combined strategy of BM-MSC transplantation with hBMP-7 gene therapy could be a useful approach for the treatment of renal IRI.

Prevalence and risk factors of peripheral arterial diseases in male Chinese octogenarians and nonagenarians with hypertension.

OBJECTIVE: To investigate the prevalence and risk factors of peripheral arterial disease (PAD) in male Chinese octogenarians and nonagenarians with hypertension. METHODS: Ankle-brachial index (ABI) was measured in the noninvasive vascular laboratory for hypertensive male octogenarians and nonagenarians enrolled from outpatient and inpatient departments. The baseline conditions were investigated using standard questionnaire and by routine physical examinations. PAD was diagnosed when an ABI≤0.9 in either lower extremity. RESULTS: Totally 290 male Chinese octogenarians and nonagenarians [age: (84.61±4.20) years] with hypertension who were receiving antihypertensive therapy were enrolled in this study, among whom 9 men with missing data except age and ABI measurements. The ABI was 0.948±0.258, with the range of highest frequency of 0.91-1.30, and 106 patients were diagnosed as PAD, 182 as non-PAD, and 2 had ABI>1.3. ABI in hypertensive men with PAD were significantly lower than in those without PAD (P<0.05). On the contrary, age, blood urea nitrogen, white blood cell counts, platelets and aspartic transaminase were significantly higher in PAD patients than in non-PAD patients (all P<0.05). The prevalence of PAD in this study population were 36.5%; more specifically, it significantly differed between different subgroups when stratified by age (28.6% vs. 46.3%, below and above 85 years), with and without hypertension (27.5% vs. 40.1%), stroke (44.7% vs. 27.5%), dyslipidemia (41.4% vs. 33.3%), coronary artery disease (44.1% vs. 13.9%), and diabetes mellitus (53.7% vs. 21.8%) (all P<0.05). The prevalences of PAD in hypertensive patients treated with diuretics, calcium antagonists, beta-blocker, or angiotensin receptor antagonist were 41.4%, 36.1%, 22.4%, and 26.8%, respectively. No association was observed between the prevalence of PAD and smoking/alcohol drinking in these subjects. Multivariate analysis showed that age (OR 1.12, 95%CI 1.014-1.238), blood urea nitrogen (OR 1.15, 95%CI 1.025-1.301), aspartic transaminase (OR 1.05, 95%CI 1.005-1.089), diabetes mellitus (OR 4.02, 95%CI 1.797-9.009), coronary artery disease (OR 6.34, 95%CI 1.734-23.214) were strong risk factors of PAD. CONCLUSION: PAD is highly prevalent among aged Chinese hypertensive men, in which age, blood urea nitrogen, aspartic transaminase, diabetes mellitus, coronary artery disease may be involved in the development of this condition.

[Clinical analysis of 6 cases of systemic lupus erythematosus complicated by transverse myelitis].

OBJECTIVE: To summarize the clinical features and therapeutic approach of systemic lupus erythematosus (SLE) complicated by transverse myelitis (TM). METHODS: The clinical characteristics, laboratory examinations, treatment and prognosis of 6 SLE cases with TM were retrospectively analyzed with review of the literatures. RESULTS: The 6 patients consisted of 5 females and 1 male aged 14 to 36 years (mean 23 years). The mean duration from symptom onset of SLE to TM was 8 months (1 to 13 months). All the patients had lower limb hypodynamia, and 3 of them developed upper limb hypodynamia. MRI scanning of the spine identified lesions in the cervical spinal cord in 2 cases, thoracic lesions in 3 cases, and multiple involvement of the cervical, thoracic and lumbar cord in 1 case. Examination of the cerebrospinal fluid yielded no specific findings except for leukocytosis in 1 case and hypoglycemia in another. Five cases were treated with high-dose MP+CTX, and the other case was treated with MP (80 mg/day)+CTX. Five patients responded favorably to the treatment, while the other showed no obvious improvement. CONCLUSION: TM is a rare complication of SLE affecting mostly young patients and occurring in the early stage of the disease. Early diagnosis and aggressive treatment might improve the prognosis.

HIV-negative drug addict diagnosed with AIDS and tuberculosis at autopsy: a case report and brief review of literature.

Human Immunodeficiency Virus (HIV) infection is a true plague and a major health concern globally. It is one of the most significant pandemics in recorded history. Despite worldwide efforts to fight the pandemic, and now with the re-emergence of tuberculosis, those clinicians, personnel performing autopsies and medical caregivers are again at risk in the work place, especially in developing countries. We describe a case where a drug abuser, whose addiction was concealed by his parents, died in hospital. He was tested HIV-negative there. A medical tangle ensued and forensic autopsy was carried out. Autopsy confirmed he was an intravenous drug addict and had tuberculosis. Post-mortem blood was positive for HIV antibodies and he was diagnosed with AIDS. Due to social stigmas, lack of knowledge or inefficient medical laboratory procedures etc, such type of cases can become a hazard to those attending the sick and to autopsy pathologists alike. We provide the case description, autopsy findings and review of pertinent literature.