The clinical characteristics and radiological data of 6 cases of sacral agenesis in one single family were analyzed and a literature review was performed.On magnetic resonance imaging (MRI),all of them presented with a partial absence of sacral vertebra,including associations with lumbar abnormalities (n =2) and sacral agenesis (n =2).One case presented with fourth/fifth lumbar vertebra bone fusion and fifth lumbar/first sacral vertebra bone fusion.On radiology,4 cases had concurrent scoliosis.None of them had tethered cord,diastematomyelia or meningocele.The understanding of sacral agenesis may be improved after reviewing and summarizing clinical features and radiological findings.

OBJECTIVEThis study aims to observe the expression of Sclerostin during movement of orthodontic teeth and determine the effect of this protein on remodeling of periodontal tissues.

METHODSTwenty-four Wistar rats were chosen. Orthodontic forces were applied between the bilateral incisor and first molar to achieve mesial movement. Rats in each group were executed at different time points (0, 1, 3, 5, 7, 14 d). Morphology of periodontal tissue was observed by hematoxylin-eosin (HE) staining. The number of osteoclasts were observed by tartrate-resistant acid phosphatase (TRAP) staining. Sclerostin expression were observed by immunohistochemical staining.

RESULTSHE staining revealed that the resorption of alveolar bone intensified with prolonged movement. Results of immunohistochemical and TRAP staining revealed that Sclerostin expression and number of osteoclasts were related to duration of movement of orthodontic tooth. After staining for 5 days, the number of osteoclasts and Sclerostin expression reached their peak and then began to decline. The numbers of osteoclasts and the expression level of Sclerostin were higher at the compressive side than those at the tensive side.

CONCLUSIONSclerostin affected orthodontic tooth movement by inhibiting the Wnt signaling pathway and by indirectly or directly controlling bone morphogenetic protein.

Animals ; Bone Morphogenetic Proteins ; metabolism ; Genetic Markers ; Incisor ; Molar ; Movement ; Osteoclasts ; Periodontal Ligament ; metabolism ; Periodontium ; Rats ; Rats, Wistar ; Tooth Movement Techniques

Objective To investigate the role and underlying mechanism of cathepsin B in myocar-dial injury in mice with diabetic cardiomyopathy(DCM).Methods Twenty 8-week-old male SPF C57BL/6 mice were randomly divided into wild-type(WT)group and WT DCM group,with 10 mice in each group.Another 20 8-week-old male SPF-grade mice with cathepsin B knockout(KO)were randomly and equally assigned to KO group and KO DCM group.HE staining was used to observe morphological changes,Prussian blue staining was employed to detect iron deposition,while immunohistochemical staining with 4-hydroxynonenal(4-HNE)was used to assess lipid peroxidation level in the myocardial tissues.Western blotting was performed to detect the expression of heme oxygenase-1(HO-1),superoxide dismutase 2(SOD2),and nuclear factor E2-related factor 2(Nrf2),while RT-PCR was applied to evaluate the expressions of Nrf-2,HO-1,and phospholipid hydroperoxide glutathione peroxidase 4(GPX4).Results Compared to the WT DCM group,the KO DCM group presented improved cell arrangement in cardiac tissues and sig-nificant reduction in inflammatory cell infiltration.Furthermore,the KO DCM group displayed a significant decrease in iron deposition compared to the WT DCM group.Additionally,the KO DCM group exhibited a significant reduction in 4-HNE expression compared to the WT DCM group.The protein levels of Nrf2,SOD2,and HO-1 were significant increased in the KO DCM group than the WT DCM group(0.68±0.21 vs 0.39±0.13,0.59±0.10 vs 0.28±0.09,1.03±0.10 vs 0.48±0.04,P＜0.05).Moreover,elevated mRNA levels of GPX4,Nrf2 and HO-1 were also observed in the KO DCM group than the WT DCM group(0.65±0.09 vs 0.40±0.10,0.61±0.11 vs 0.34±0.11,0.62±0.12 vs 0.39±0.09,P＜0.05).Conclusion Cathepsin B exacerbates myocardial injury in DCM mice through ferroptosis.

Objective To compare the differences in the long-term survival rate and the tumor shrinkage rate of inoperable hepatocellular carcinoma (HCC) between transcatheter arterial chemoembolization (TACE) combined with percutaneous ablation therapy and simple TACE therapy in order to provide the basis for the clinical treatment of HCC.Methods Randomized controlled trials (RCT) for comparing the difference in survival rates between TACE plus PA and simple TACE for inoperable HCC were searched from medical literature database,from which the relevant data were extracted.According to Cochrane manual standard,the quality of inclusion literature was evaluated.Results A total of 15 RCT papers were included in this study,including 859 HCC patients.The results of meta-analysis showed that all the 1-year,2-year and 3-year survival rates in TACE plus PA group were better than those in simple TACE group (RR=1.454,95％CI=1.333and 1.586,Z=8.56,P＜0.001;RR=1.781,95％CI=1.511 and 2.099,Z=6.88,P＜0.001;RR=2.351,95％CI=1.808 and 3.059,Z=6.37,P＜0.001,respectively).The tumor shrinkage rate in TACE plus PA group was also better than that in simple TACE group (RR=1.314,95％CI=1.190 and 1.452,Z=5.38,P＜0.001).The sensitivity analysis indicated that the results of the differences in survival rate and tumor shrinkage rate between the two groups were reliable.Conclusion The 1-year,2-year and 3-year survival rates as well as the tumor shrinkage rate of TACE plus PA group are higher than those of simple TACE group.

Leptin is a protein hormone produced mainly by obese gene and secreted by adipose tissue and exerts the biological effects through leptin receptors. With the progress in research on the function and receptor signal transduction related leptin and leptin resistance, it has been found that leptin is associated with the development and progression of many cardiovascular diseases, such as hypertension and left ventricular hypertrophy. Some studies have reported that leptin resistance is the pathologic basis for a variety of cardiovascular diseases. This paper will briefly review the advances in the study of correlation between leptin and hypertensive-left ventricular hypertrophy (HLVH), focusing on the relationship between leptin and various factors related to HLVH, such as sympathetic nervous system, renin angiotensin aldosterone system, growth factors, inflammatory factors and insulin resistance.
Adipose Tissue ; Cardiovascular Diseases ; Humans ; Hypertension ; Hypertrophy, Left Ventricular ; Insulin Resistance ; Leptin ; physiology ; Receptors, Leptin ; Renin-Angiotensin System ; Sympathetic Nervous System

Lung cancer is the leading cause of cancer-related deaths. Traditional chemotherapy causes serious toxicity due to the wide bodily distribution of these drugs. Curcumin is a potential anticancer agent but its low water solubility, poor bioavailability and rapid metabolism significantly limits clinical applications. Here we developed a liposomal curcumin dry powder inhaler (LCD) for inhalation treatment of primary lung cancer. LCDs were obtained from curcumin liposomes after freeze-drying. The LCDs had a mass mean aerodynamic diameter of 5.81 μm and a fine particle fraction of 46.71%, suitable for pulmonary delivery. The uptake of curcumin liposomes by human lung cancer A549 cells was markedly greater and faster than that of free curcumin. The high cytotoxicity on A549 cells and the low cytotoxicity of curcumin liposomes on normal human bronchial BEAS-2B epithelial cells yielded a high selection index partly due to increased cell apoptosis. Curcumin powders, LCDs and gemcitabine were directly sprayed into the lungs of rats with lung cancer through the trachea. LCDs showed higher anticancer effects than the other two medications with regard to pathology and the expression of many cancer-related markers including VEGF, malondialdehyde, TNF-, caspase-3 and BCL-2. LCDs are a promising medication for inhalation treatment of lung cancer with high therapeutic efficiency.

OBJECTIVE: To construct a HIV-1 gp120 transgenic mouse model (gp120) with 7 nicotinic acetylcholine receptor (7nAChR) gene knockout. METHODS: The 7nAChR gene knockout mice (7R) were crossed with HIV-1gp120 transgenic mice (gp120) to generate F1 generation mice. We selected the F1 mice with the genotype of 7R/gp120 to mate to obtain the F2 mice. The genotypes of the F3 mice were identified by PCR, and the protein expressions in the double transgenic animal model was analyzed by immunohistochemistry. BV2 cells were treated with gp120 protein and 7nAChR inhibitor, and the expressions of IL-1β and TNF- were detected using ELISA. RESULTS: The results of PCR showed the bands of the expected size in F3 mice. Two F3 mice with successful double gene editing (7R/gp120) were obtained, and immunohistochemistry showed that the brain tissue of the mice did not express 7 nAChR but with high gp120 protein expression. In the cell experiment, treatment with gp120 promoted the secretion of IL-1β and TNF- in BV2 cells, while inhibition of 7nAChR significantly decreased the expression of IL-1β and TNF- ( < 0.001). CONCLUSIONS By mating gp120 Tg mice with 7R mice, we obtained gp120 transgenic mice with 7nAChR gene deletion, which serve as a new animal model for exploring the role of 7nAChR in gp120-induced neurotoxicity.
Animals ; Disease Models, Animal ; Glycoproteins ; Mice ; Mice, Knockout ; Mice, Transgenic ; Tumor Necrosis Factor-alpha ; alpha7 Nicotinic Acetylcholine Receptor ; metabolism

Objective To understand the distribution of novel coronaviruses in the external environment of confirmed COVID-19 cases. Methods Environmental surface swab specimens such as bed rails, doorknob, closestool, hand washing sink, table, locker,ward pager, mobile phone, cup, clothes, were collected from the sentinel hospital of COVID-19, and samples were collected for the nucleic acid detection by RT-PCR. Results A total of 150 environmental samples were collected from 30 confirmed COVID-19 cases, 6 samples were determined to be novel coronaviruses postive (positive rate 4.00%). The total 14 mobile phone showed 3 novel coronaviruses positive.Among the 30 confirmed COVID-19 cases, 6 cases (positive rate 20.00%)were found novel coronaviruses in the external environment. Conclusions Novel coronaviruses exists in external environment of confirmed COVID-19 cases, which indicates the potential risk of COVID-19 infection.

OBJECTIVETo observe the curative effect and side effect of tigecycline in the treatment of patients with infection caused by granulocytopenia.

METHODSThe clinical data of 107 patients who were treated with tigecycline for infection due to granulocytopenia were retrospectively reviewed. The tigecycline was administered by intravenously (30-60 min drip infusion)as the initial dose of 100 mg and maintenance does of 50 mg, every 12h. The whole treatment course kept for 5-7 d when the body temperature was normal and then the step-down treatment or discontinuation of the drug was adopted.

RESULTSA total of 104 strains of bacteria were isolated from 107 cases of hospitalized patient, including 60 multi-drug resistant strains (MDR) and 2 extensively-drug resistant strains (XDR). The total effective rate of tigecycline treatment was 62.6%, including 30 cases with tigecycline alone (63.3% of the effective rate), 21 cases with tigecycline as initial treatment followed by combination with other antibiotics (61.9% of the effective rate), and 56 cases with tigecycline in combination with other antibiotics from the beginning of the treatment (62.5% of the effective rate). There was no statistical significant difference between the 3 treatment groups (P=0.994). Among the 39 patients with MDR strains, 22 patients' temperature was controlled , 9 patients died, and 8 patients' temperature remained uncontrolled. The clinical effective rate of these patients was 56.4%. The median onset time of tigecycline treatment was 3 days. The adverse drug reactions of nausea (11.2% ) and vomiting (8.4% )were tolerable.

CONCLUSIONTigecycline is effective in treatment of resistant bacteria infection in patients with granulocytopenia. The side effects of tigecycline were few, safe and generally well tolerated.

Agranulocytosis ; complications ; microbiology ; Anti-Bacterial Agents ; therapeutic use ; Bacterial Infections ; drug therapy ; Body Temperature ; Drug Resistance, Multiple, Bacterial ; Humans ; Minocycline ; analogs & derivatives ; therapeutic use ; Retrospective Studies ; Treatment Outcome

Although genome-wide association studies have identified more than eighty genetic variants associated with non-small cell lung cancer (NSCLC) risk, biological mechanisms of these variants remain largely unknown. By integrating a large-scale genotype data of 15 581 lung adenocarcinoma (AD) cases, 8350 squamous cell carcinoma (SqCC) cases, and 27 355 controls, as well as multiple transcriptome and epigenomic databases, we conducted histology-specific meta-analyses and functional annotations of both reported and novel susceptibility variants. We identified 3064 credible risk variants for NSCLC, which were overrepresented in enhancer-like and promoter-like histone modification peaks as well as DNase I hypersensitive sites. Transcription factor enrichment analysis revealed that USF1 was AD-specific while CREB1 was SqCC-specific. Functional annotation and gene-based analysis implicated 894 target genes, including 274 specifics for AD and 123 for SqCC, which were overrepresented in somatic driver genes (ER = 1.95, P = 0.005). Pathway enrichment analysis and Gene-Set Enrichment Analysis revealed that AD genes were primarily involved in immune-related pathways, while SqCC genes were homologous recombination deficiency related. Our results illustrate the molecular basis of both well-studied and new susceptibility loci of NSCLC, providing not only novel insights into the genetic heterogeneity between AD and SqCC but also a set of plausible gene targets for post-GWAS functional experiments.
Adenocarcinoma of Lung/genetics* ; Carcinoma, Non-Small-Cell Lung/genetics* ; Carcinoma, Squamous Cell/genetics* ; Genetic Heterogeneity ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Lung Neoplasms/genetics* ; Polymorphism, Single Nucleotide