[Surgical treatment of the complex bicondylar tibial plateau fracture using a midline longitudinal incision].

Objective: To explore the outcomes after treatment of the complex bicondylar tibial plateau fracture through a midline longitudinal approach. Methods: A review of fifteen patients with an average age of (51.3±12.3) years old (range17-65yers;7 males, 8 females) surgically treated from October 2013 to Febuary 2018 were included. Sahatker Ⅴ in 10, Sahatker Ⅵ in 5; fractures of medial and lateral columns in 9, fractures of three columns in 6. All the patients were adopt a midline longitudinal approach combined with the posterior approach and bone grafting were conducted. Results: All cases were followed-up for (14.4±3.8) month, with an average of 12-24 month. All patients gained bone union during 12-16 weeks after operation, with an average of (15.2±1.3) weeks. There were significant differeces in both tibial plateau angle and posterior slope angle on radiography between preoperation and postoperation (P<0.05), there were no significant differeces in either tibial plateau angle or posterior slope angle on radiography between immediate postoperation and 12 months postoperation (P>0.05). At final follow-up,both the Lachman test and the Pivot-shift test were negative. All patients had complete knee extension, knee flexion angle 100°-135°, with an average of 117.7°±11.3°. The HSS (the Hospital for Special Surgery) score were 66-98, with an average of 85.1±9.3, six cases were excellent and seven cases were good, two cases was fair, the excellent and good rate was 86.7%. The Rasmussen radiological evaluationre were 9-18, with an average of 15.1±2.5, three cases were excellent and eleven cases were good, one cases was fair, the excellent and good rate was 93.3%. 1 patient had fat liquefactionof in antero incision, and got good outcomes after debridement dressing. Conclusion: The treatment of the complex bicondylar tibial plateau fracture through a midline longitudinal approach combined with the posterior approach can result in good exposure and satisfying knee function in short-term.

Shared genetic etiology of hypertension and stroke: evidence from bioinformatics analysis of genome-wide association studies.

Hypertension is the most significant modifiable risk factor for cerebrovascular disease. It has been estimated that about 54% of strokes worldwide can be attributed to hypertension. However, there has not been a systematic study assessing the shared genetic susceptibility to hypertension and stroke on a genome-wide level. In this study, SNPs associated with essential hypertension and stroke were collected from the NHGRI-EBI GWAS catalog, and genotype imputation were conducted using information from the 1000 Genomes Project. Subsequently, the SNPs and the mapped genes were compared between the two diseases. Finally, functional clustering was performed, and the enriched GO terms and KEGG pathways were further compared between hypertension and stroke. Comparison of these two groups of SNPs and genes identified only one shared SNP (rs3184504) and 11 shared genes. After genotype imputation, 129 shared SNPs and 16 shared genes were identified. These genes were significantly enriched in 10 GO terms, which were mainly involved in lipoprotein and triglyceride metabolism. Additionally, KEGG analysis identified one pathway, glycerolipid metabolism, as being significantly enriched in both diseases. The present study strongly suggests that the gene network regulating lipid metabolism and blood circulation is the major shared genetic etiology of hypertension and stroke.

Are genetic polymorphisms in the renin-angiotensin-aldosterone system associated with essential hypertension? Evidence from genome-wide association studies.

In candidate gene era, dozens of single-nucleotide polymorphisms (SNPs) within renin-angiotensin-aldosterone system (RAAS) have been reported to be significantly associated with hypertension. However, the unbiased genome-wide association studies (GWAS) rarely identified the SNPs within RAAS were associated with hypertension or blood pressure (BP) traits. In order to figure out whether genetic polymorphisms of RAAS are really associated with hypertension, we systemically searched the GWAS Catalogue and identified all the known RAAS genes and relevant diseases/traits. After data processing, we found that polymorphisms within REN, AGT, ACE2, CYP11B2, ATP6AP2 and HSD11B2 were not associated with any disease or trait. SNPs within ACE, AGTR1, AGTR2, MAS1, RENBP and NR3C2 were associated with other diseases or traits, but showed no direct connection with hypertension. The only SNP associated with a BP trait, systolic BP was rs17367504. However, it is located in the intronic region of MTHFR near many plausible candidate genes, including CLCN6, NPPA, NPPB and AGTRAP. Therefore, the effect of RAAS polymorphisms may have been overestimated during the 'candidate gene era'. In the time of 'precision medicine', the power of RAAS variants needs to be reconsidered when evaluating one's susceptibility of hypertension.

Inflammation in lung after acute myocardial infarction is induced by dendritic cell-mediated immune response.

The present study was performed to describe the changes of lung tissues in mice with acute myocardial infarction (AMI) and also explain the cell mechanism involved in inflammation in lung. AMI was established by left coronary ligation in mice. Then mice were divided into three groups: control group, MW1 group (sampling after surgery for one week) and MW2 group (sampling after surgery for two weeks). Afterwards, measurement of lung weight and lung histology, cell sorting in bronchoalveolar lavage (BAL) fluid and detection of several adhesive molecules, inflammatory molecules as well as enzyme associated with inflammation were performed. Moreover, dendritic cells (DCs) were isolated from bone marrow of C57B/L6 mice. After incubating with necrotic myocardium, the expression of antigen presenting molecules, co-stimulatory molecules and inflammatory molecules were detected by flow cytometry or immunohistochemistry in DCs. We also detected T-cell proliferation after incubating with necrotic myocardium-treated DCs. AMI induced pathological changes of lung tissue and increased inflammatory cell amount in BAL fluid. AMI also increased the expression of several inflammatory factors, adhesive molecules and enzymes associated with inflammation. CD11c and TLR9, which are DC surface markers, showed a significantly increased expression in mice with AMI. Additionally, necrotic myocardium significantly increased the expression of co-stimulatory factors including CD83 and CD80, inflammatory cytokines including TNF-α, IFN-γ and NF-κB in DCs. Furthermore, DCs treated with necrotic myocardium also significantly promoted T-cell proliferation. AMI induced inflammation in lung and these pathological changes were mediated by DC-associated immune response.

Genome-wide profiling reveals epigenetic inactivation of the PU.1 pathway by histone H3 lysine 27 trimethylation in cytogenetically normal myelodysplastic syndrome.

Cytogenetically normal myelodysplastic syndrome (CN-MDS) can pose diagnostic challenges and its pathogenetic mechanism remains elusive. By focusing on cytogenetically normal refractory cytopenia with multilineage dysplasia (CN-RCMD), a subtype of MDS, our genome-wide profiling showed ∼4600 annotated gene promoters with increased Histone H3 lysine 27 trimethylation (H3K27me3) in CN-RCMD, when compared with normal controls. Computational analysis revealed a statistically significant enrichment of the PU.1-binding DNA motif (PU-box) in the regions with increased H3K27me3. An inverse relationship between the levels of H3K27me3 and the levels of PU.1 binding and its downstream myeloid gene expressions was observed. Whole-exome sequencing analysis and Sanger sequencing analysis revealed some recurrent mutations, but no mutations in the PU.1 regulatory regions or in the EZH1/2, H3K27 methytransferase encoding genes. Using an MDS-derived erythroid/myeloid line and primary MDS bone marrow cells, we demonstrated that H3K27me3 inhibitors can increase the expression of PU.1 and its downstream genes and also promote cell differentiation via reducing H3K27me3 at the PU.1 gene locus. Finally, ectopic expression of PU.1 significantly inhibited proliferation of the MDS-derived cell line. Based on these data, we propose a hypothetical model of epigenetic inactivation of the PU.1 pathway due to increased H3K27me3 in some cases of CN-RCMD.

Screening for liver cancer: results of a randomised controlled trial in Qidong, China.

OBJECTIVES: To investigate the effectiveness of screening for liver cancer in reducing mortality from the disease in a high-risk population in China. SETTING: A randomised controlled trial was carried out among men aged 30-69 who were chronic carriers of hepatitis-B virus (HBsAg positive) during the period 1989-1995 in Qidong county, Jiangsu Province, China. METHODS: 5581 HBsAg carriers were identified by population screening and randomly assigned to a screening group (group A, 3712 men), and controls (group B, 1869 men). Screening was planned to be six monthly alpha-fetoprotein (AFP) assays, with follow-up of subjects having an abnormal (>/=20 micrograms/l) test. All subjects were followed up for liver cancer and/or death until 31 December 1995. RESULTS: The overall sensitivity and specificity of the programme was 55.3% and 86.5%, respectively; in subjects who complied with all scheduled screening tests, the values were 80.0% and 80.9%. Three hundred and seventy-four primary liver cancer (PLC) cases were diagnosed. The percentage of cases in stage I was significantly higher in group A (29.6%) than in group B (6.0%). The one-, three-, and five-year relative survival rates were 23.7%, 7.0%, and 4.0% in group A, and 9.7%, 4.0%, and 4.1% in group B respectively, with no difference in five-year survival between the groups. The mortality rate in the screened group (1138 per 100,000 person-years) was not significantly different from that in the controls (1114 per 100,000). A Poisson regression model showed that the probability of death (rate ratio) in the screening group was 0.83 (95% CI 0.68-1.03) relative to the control group. CONCLUSIONS: Screening with AFP resulted in earlier diagnosis of liver cancer, but the gain in lead time did not result in any overall reduction in mortality, because therapy for the patients found by screening was ineffective. Further studies using improved methods of screening, diagnosis and treatment are indicated.

Association of distal chromosome 2q with IDDM in Japanese subjects.

An insulin-dependent diabetes mellitus (IDDM)-susceptibility gene (IDDM13) has recently been mapped to a region of distal chromosome 2q, which is syntenic to the region of mouse chromosome 1 containing a murine susceptibility gene for IDDM, Idd5. To determine the contribution of this region to IDDM disease susceptibility further and to narrow the region for positional cloning of susceptibility genes, we have studied the association of distal chromosome 2q with IDDM in the genetically distinct Japanese population. A 137 mobility unit (mu) allele at D2S137 locus was significantly associated with IDDM (odds ratio 1.92, p = 0.0016). Other markers, D2S301 and D2S143, located in the same region were not associated with IDDM, indicating that IDDM13 is in linkage disequilibrium with D2S137, but not with D2S301 or D2S143. The association of D2S137 with IDDM was observed in patients lacking one of two high risk HLA alleles, DQBI*0303 and DQBI*0401, but not in patients with either of these alleles. The frequency of high risk HLA alleles was significantly lower in patients with the susceptible allele at D2S137, suggesting that IDDMI3 contributes to IDDM susceptibility in subjects without high risk genotypes at IDDM1. Demonstration of allelic association of D2S137 with IDDM localizes IDDM13 in the close vicinity (<2 centiMorgans) of D2S137, greatly facilitating fine structure mapping and positional cloning of IDDM13.

Styles of verbal expression of emotional and physical experiences: a study of depressed patients and normal controls in China.

Sixty depressed patients and 52 normal controls completed three selfreport inventories: the Symptom Checklist-90 (SCL-90), the Beck Depression Inventory (BDI) and a new Verbal Style Investigation Schedule (VESIS) developed by the first author. The VESIS uses 16 key emotional and physical terms from Western inventories and identified the words and phrases most commonly used by Chinese patients to express these feeling states. Chinese subjects commonly used the key term itself for only 3 or the 16 key terms; they usually preferred to use other words or phrases to express the feeling state. We categorized these Chinese expressions into four styles of verbal expression: Psychological, Somatic, Neutral (i.e., a mixture of psychological and somatic) and Deficient (i.e., lack of expression because of denial or suppression). Three of the 12 key emotional terms of the VESIS (depressed, fearful, and anxiousness) were more commonly expressed in a somatic or neutral mode than the other key emotional terms. The key terms "suicidal interest" and "being punished" were more commonly expressed in a deficient style than other key emotional terms. The somatic factor score of the SCL-90 was not correlated with increased somatic expression of emotional states; thus patients who have multiple somatic complaints are not more likely to express emotions somatically. The hypothesis of somatization is discussed in light of this study.