Objective: To observe the effect of modified myocutaneous flaps in the treatment of lower eyelid relaxation. Methods: From June 2017 to November 2018, 85 patients with lower eyelid relaxation were treated in our hospital. Modified musculocutaneous flaps were used in all cases. The techniques of preservation of eye fur, treatment of lacrimal grooves and muscle resection and suture were emphasized during the operation. All patients were followed up for 6 months to observe the occurrence of complications. At 6 months after operation, the satisfaction of operation was evaluated. Results: After 6 months of follow-up, 79 cases (92.94%) were satisfied. The symptoms included the disappearance of lower eyelid skin relaxation, the disappearance of lower eyelid margin baggy groove, no eyelid retraction, the formation of " orbicularis oculi muscle threshold" on the eyelid margin, and no obvious scar. There were 6 cases of basic satisfaction and 0 cases of unsatisfactory. Two patients had mild eyelid ectropion, 2 patients had slight scar hyperplasia at the lateral canthus incision, and no complications such as retrobulbar hematoma, infection and facial nerve injury occurred. No second repair operation was performed. Conclusions Modified musculocutaneous flaps have a satisfactory effect in the treatment of lower eyelid skin relaxation. It not only takes into account the advantages of the two traditional methods of skin flaps and musculocutaneous flaps, but also retains the natural physiological curvature of eye fur. It can also significantly improve the wrinkles and lacrimal grooves of lower eyelid. It is worthy popularizing.

Objective To summarize CT and MRI features of hyaline vascular type localized Castleman disease(LCD)and analyze the causes of misdiagnosis,to improve the preoperative diagnosis rate.Methods The clinical and imaging data of 7 patients with hyaline vascular type LCD confirmed by operation and pathology were analyzed retrospectively.Results (1)6 cases were misdiagnosed before operation,1 case was misdiagnosed as pancreatic neuroendocrine tumor,1 case as thymoma,1 case as neurogenic tumor,1 case as pheochromocytoma, 1 case as clear cell renal cell carcinoma and 1 case as small mesenteric stromal tumor.(2)1 case was located in the right neck,1 case in the anterior superior mediastinum,1 case in the neck of the pancreas,1 case in the upper part of the left kidney,2 cases in the retroperitoneum and 1 case in the lower abdomen.(3)3 cases were scaned by dynamic enhanced MRI,3 cases were scaned by dynamic enhanced CT, and 1 case was checked by plain CT and enhanced MRI.CT and MRI showed that 7 cases had a round or elliptical soft tissue mass, and 4 cases with well defined margin,3 cases were not clear in edge,2 cases with spot or strip calcification on CT images,4 cases had slightly longer T1 and longer T2 signal,4 cases were restricted of diffusion and had higher signal on DWI.All the lesions were enhanced in arterial phase,and went on in the delayed phase.There were 5 cases with distorted vascular shadow in the middle and/or around of the mass, 3 cases with strips,spoke-like low-density areas or low-signal areas,and some lesions were filled in delayed phase.Conclusion CT and MRI features of hyaline vascular type LCD have certain characteristics such as rich blood supply,enhancement in persistent,tortuosity of peripheral vascular,with some short strip calcification and high signal on DWI,which may be helpful for preoperative diagnosis.

The cases of paradoxical brain embolism (PBE) due to venous aneurysms and patent foramen ovale (PFO) are extremely scarce, with only 5 cases caused by popliteal venous aneurysm reported in the literature to date, while PBE caused by deep femoral venous aneurysm (DFVA) and PFO has not been reported. Herein, an unusual case of PBE in a 15-year-old girl with PFO who still had cerebral infarction and pulmonary embolism after transcatheter closure was present. She was finally diagnosed as PFO with DFVA by angiography. Furthermore, clinical characteristics of 6 cases were summarized to improve the clinicians′ recognition of the rare risk factor of stroke-venous aneurysms of the lower extremity deep veins.

Objective:To determine the content of Chikusetsu saponin Ⅳa in the roots, stems and leaves in Panacis japonici rhizoma, and explore its development value. Methods:By using High Performance Lliquid Chromatography (HPLC) method to determine the content of Chikusetsu saponin Ⅳa in the roots, stems and leave of Panacis japonici rhizoma. Inertsil ODS-sp (4.6 mm×150 mm, 5 μm) was used as the column and the acetonitrile-0.2% phosphoric acid (35:65) as the mobile phase. The flow rate was 1 ml/min with the temperature 35 ℃ under wavelength 210 nm. Results:The linear ranged from 1-10 μg of Chikusetsu saponin Ⅳa was good ( r=0.999 5). The content of Chikusetsu saponin Ⅳa in the roof, stem and leaf were 2.169%, 0.269%, 0.169%, respectively. Conclusions:The roof of Panacis japonici rhizoma contains the highest level of Chikusetsu saponin Ⅳa followed by stem and leaf. The roof part could be used as the medical part and its stem and leaf are also valuable for further development.

Objective To summarize the pathological survey of time-zero renal biopsy (T0-RBx ) . Methods The material qualities and pathological features were analyzed retrospectively for T 0-RBx (n=176) between March 2008 and May 2016 .According to the source of donor kidney ,T0-RBx specimens were divided into living donors (LD) group (n=137) and Deceased donation (DD) group (n=39) .Furthermore , the DD group was divided into cerebral hemorrhage group (n= 10) and brain trauma group (n= 29) according to the causes of death .The inter-group differences of pathological characteristics and the effects of abnormal pathological lesions on allograft function were observed .Results All T0-RBx specimens contained cortical kidney tissue .The average microscopic length of renal tissue was (0 .39 ± 0 .23) cm and the median glomerular number 11 . The abnormal pathological lesions included glomerulosclerosis (GS ,30 .7 ％ ) , segmental glomerulosclerosis (1 .1 ％ ) ,mesangial increase (MI ,19 .3 ％ ) ,tubular atrophy (TA ,35 .2 ％ ) , acute tubular necrosis (ATN ,9 .1 ％ ) ,vacuolar degeneration of tubular epithelium (27 .3 ％ ) ,losses in tubule epithelial brush border (97 .7 ％ ) , protein cast (25 ％ ) , interstitial fibrosis (IF ,34 .1 ％ ) , inflammation (I ,42 .6 ％ ) ,arteriolar hyalinosis (AH) (26 .1 ％ ) and vascular fibrous intimal thickening (CV ,23 .3 ％ ) .Among them ,23 .9 ％ ,1 .1 ％ ,0 .55 ％ and 0 .55 ％ cases were diagnosed as IgA nephropathy ,immune complex associated with glomerular disease and focal segmental glomerulosclerosis diabetic nephropathy respectively .And the reminders were of ischemic injury .The incidence rates of TA ,IF and I were lower in DD group than those in LD group ( P< 0 .05 ) . However , ATN and vacuolar degeneration of tubular epithelium were higher (P<0 .001) .The incidence of GS was significantly higher in cerebral hemorrhage group than that in brain trauma group (P<0 .01) .No statistical difference existed in other lesions or disease constitution among the groups (P>0 .05) .Further analysis showed GS was related with allograft function at 6/12 months post-transplantation in both LD and DD groups (P<0 .05) .IF and AH were also related to short-term renal function of recipients post-transplantation in LD and DD groups (P>0 .05) .Conclusions T0-RBx may detect the abnormal lesions of donor kidney .Some differences exist in types and degree of abnormal lesions among different donor kidneys .LD group has a higher risk for chronic histological injury such as TA and IF while DD group is more susceptible to acute renal tubular interstitial injury .Thus it is valuable for predicting allograft function post-transplantation .Material quality is essential for ensuring the reliability of T 0-RBx .

Objective: To investigate the effect of G protein-coupled receptor 108(GPR108) gene knockout on systemic inflammation in lipopolysaccharide(LPS)-induced sepsis mice. Methods: Male C57BL/6 mice and GPR108 gene knockout mice were randomly divided into 4 groups: WT group, WT-LPS group, KO group, KO-LPS group. The physiological characteristics of mice in different groups were observed, and the morphological changes of liver and lung tissues were observed. Macrophages were extracted from bone marrow and subjected to flow cytometry to detect their M1 polarization status. The expression levels of IL-6 in liver and lung tissues, macrophages, and serum were also measured. Results: KO-LPS group mice showed significant liver and lung tissue damage, with a significantly greater number of bone marrow-derived macrophages polarizing towards M1 in the KO-LPS group compared to the WT-LPS group. Additionally, at the tissue, cellular, and serum levels, the expression of IL-6 in the KO-LPS group mice was significantly higher than that in the WT-LPS group mice(P<0.05). Conclusion During the systemic inflammatory infection induced by LPS in mice, the lack of GPR108 exacerbates the systemic inflammatory response. GPR108 has an inhibitory effect on the inflammatory response in mice with LPS-induced sepsis.

Objective: To establish a Tohoku hospital pediatrics-1 (THP-1) cell line with G protein-coupled recep- tor108 ( GPR108) deletion and explore its functions． Methods: According to the requirements of the clustered regularly interspaced short palindromic repeats ( CRISPR) / CRISPR-associated protein 9 ( Cas9 ) system ，two single guide RNAs (sgRNA1 and sgRNA2) paring to the flanking fragments of human GPR108 gene were designed and synthesized．The two oligonucleotides were inserted in the pL-CRISPR. EFS．GFP vector to generate the new recombinant vectors ( pL-CRISPR. EFS．GFP-sgRNA1 and pL-CRISPR. EFS．GFP-sgRNA2 ) ．The recombinant vectors and packaging plasmids (pMD2. G and psPAX2) ，were co-transfected into 293T cells to generate virus for infecting THP-1 cells．The GFP + cells were screened and isolated in 96-well culture plates by flow cytometry to obtain single-cell clones．PCR and Western blot were used to detect whether GPR108 was successfully knocked out in THP- 1 cells．Both GPR108 + / + and GPR108 －/ － THP-1 cells were treated with lipopolysaccharide (LPS) ．Interleukin 8 (IL-8) derived from the THP-1 cells，which were treated by LPS，was detected with Western blot and cytometric bead array ( CBA) analysis. Results: The recombinant lentiviral vector pL-CRISPR. EFS．GFP-sgRNA was successfully constructed and single-cell clone F9 was obtained by flow cytometric sorting after transfection of THP-1 cells．PCR and Western blot both confirmed that F9 was a GPR108 －/ － THP-1 single-cell clone． LPS stimulated GPR108 －/ － and GPR108 + / + THP-1 cells，both Western blot and CBA results showed a significant decrease in IL- 8 synthesis and secretion in GPR108 －/ － THP-1 cells． Conclusion The GPR108 －/ － THP-1 cell clone is success- fully obtained based on the CRISPR / Cas9 system．GPR108 deletion in THP-1 cells treated by LPS leads to a decrease of IL-8 expression and secretion．It lays the foundation for further research on the molecular mechanisms of GPR108 in the immune inflammatory response.

Objective: To investigate the role and mechanism of Sigirr deletion in chronic kidney disease complicated with renal interstitial fibrosis (CKD⁃RIF) in mice. Methods: polymerase chain reaction (PCR) was used for identification of gene types of mice. Mice were continuously fed with the foods containing 0. 2% adenine for 12 weeks to establish the CKD⁃RIF models. Then , serum was collected to detect levels of creatinine and nitrogen when mice were killed. H&E staining was used to analyze the pathological changes of kidney tissues. Masson staining was used to observe the degree of renal fibrosis. Immunohistochemistry was used to detect the changes of the interest proteins , such as IL⁃1β , MyD88 , activated NF⁃κB , TGF⁃ β1 , E ⁃cadherin and Vimentin. Results: Serum creatinines and urea nitrogens of mice fed with high adenine (CKD⁃RIF groups) significantly increased , compared with those of the control groups. H&E and Masson staining results showed that there were more infiltrated inflammatory cells and more critical collagen fiber deposition in the renal tissues of the Sigirr - / - mice with CKD⁃RIF. Western blot and Immunohistochemical analysis showed that the expression of IL⁃1β and its downstream MyD88 increased , and the level of phosphorylated NF⁃κB (p⁃P65) significantly increased in the renal tissues of CKD⁃RIF mice compared with the controls. And upregulation of these proteins in renal tissues of Sigirr - / - mice with CKD⁃RIF was more obvious than that of the CKD⁃RIF Sigirr + / + mice. TGF⁃ β1 , as a key cytokine involved in renal interstitial fibrosis , significantly increased ,followed by the increase of vimentin , as well as the decrease of E ⁃cadherin . The results of vimentin and cadherin E detected by Western blot were consistent with those of immunohistochemistry , and α ⁃SMA also increased significantly. Conclusion Adenine diet successfully induces CKD⁃RIF mice models. Sigirr deletion is beneficial to activation of the IL⁃1β mediating NF⁃κB signal pathway ,which promotes TGF⁃ β1 expression in the renal interstitiums to induce renal interstitial fibrosis.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce cardiovascular mortality in patients with diabetes mellitus but the protective mechanism remains elusive. Here we demonstrated that the SGLT2 inhibitor, Empagliflozin (EMPA), suppresses cardiomyocytes autosis (autophagic cell death) to confer cardioprotective effects. Using myocardial infarction (MI) mouse models with and without diabetes mellitus, EMPA treatment significantly reduced infarct size, and myocardial fibrosis, thereby leading to improved cardiac function and survival. In the context of ischemia and nutritional glucose deprivation where autosis is already highly stimulated, EMPA directly inhibits the activity of the Na⁺/H⁺ exchanger 1 (NHE1) in the cardiomyocytes to regulate excessive autophagy. Knockdown of NHE1 significantly rescued glucose deprivation-induced autosis. In contrast, overexpression of NHE1 aggravated the cardiomyocytes death in response to starvation, which was effectively rescued by EMPA treatment. Furthermore, in vitro and in vivo analysis of NHE1 and Beclin 1 knockout mice validated that EMPA's cardioprotective effects are at least in part through downregulation of autophagic flux. These findings provide new insights for drug development, specifically targeting NHE1 and autosis for ventricular remodeling and heart failure after MI in both diabetic and non-diabetic patients.
Animals ; Diabetes Mellitus ; Diabetes Mellitus, Type 2/drug therapy* ; Glucose ; Humans ; Mice ; Myocardial Infarction/metabolism* ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use* ; Ventricular Remodeling