Objective To identify the anatomical basis for aging orbit-malar fold forming orbitmalar groove and its underlying mechanism.Methods Thirteen cadavers (26 hemifaces) were dissected in this study (9 male and 4 female heads).All specimens were fixed in 10％ formalin,with age ranges from 22 to 78 years.The lateral orbital region was dissected in layers by mieroinsrument using 10 X loupe magnification,especially at the palpebral and the lateral orbital part,and then the anatomy layer was described; the lateral orbital thickening (LOT) was performed carefully to evaluate whether there were multiple anatomical contributions to anatomy.Anatomic observations were systematically recorded,sketched,and photographically documented.Results The lateral orbital layers included skin,subcutaneous adipose tissue,orbicularis oculi muscle,middle temporal fascia,and periosteum.The lateral orbital thickening was a triangular condensation of fascia,which extended over the lateral orbital rim onto the adjacent medial tem~ral fascia,the lateral orbital thickening was measured (9.28 ±0.45) mm in transverse width from Vertex triangle to lateral canchal,the inner part of the LOT sanwiched between orbibularis and obital septum,which consisted of upper lid and lower lid part,the lower lid part presented transverse V shape,the top part of the transverse V was adhesive to fascial tissue over tarsal plate.The distance to lateral canthus angular was 21.69-37.21 mm,and the under part was adhesive to low orbital rim the low arm distance to lateral canthus angular was (13.55 ±0.52) mm.Vertex of.V to lateral canthus angular vertical distance was (11.35±0.27) mm.Conclusions The reason why aging orbit-malar fold forms orbital-malar groove is the atrophy of the subcutaneous adipose tissue and the middle temporal fascia fat.

Objective To discuss the possible molecular mechanisms involved in the protective effects of Biifdobacterium on intestinal tissue of necrotizing enterocolitis (NEC) newborn rats. Methods Seventy-five newborn Sprague-Dawley rats (born within 2 h) were randomly divided into five groups, each group with 15 rats. Group A was the NEC model group, and the rats were fed lipopolysaccharide (LPS) and formula. Group B was the Biifdobacterium treatment group, and the rats were fed LPS and formula and Biifdobacterium micro-capsule. Group C was the artificial feeding control group, and the rats were fed formula. Group D was the Biifdobacterium control group, and the rats were fed formula and Biifdobacterium micro-capsule. Group E was the breastfeeding control group, and the rats were fed rat breast milk by mothers. LPS 30 mg/kg was administered by gavage once per day for 3 days. Bifidobacterium micro-capsules were given as 1×1010 colony forming units/ml by gavage with formula once per day. After fed for 72 h and fasted for 12 h, the five groups of rats were killed by decapitation. Morphological changes in the terminal ileum tissue were observed under a light microscope and intestinal injury was scored. The expression of Toll-like receptor (TLR) 2, TLR4, and nuclear transcription factor (NF)-κB p65 was detected by immunohistochemical methods. Kruskal-Wallis test, analysis of variance, corrected Chi-square test and Fisher's exact test were used for statistics. Results The morbidity of NEC in group A to E was 11/15, 4/15, 3/15, 2/15 and 0/15, respectively;the intestinal injury score in group A to E was 3.37±0.27, 1.53±0.44, 1.75±0.37, 0.92±0.39 and 0.30±0.18, respectively; the expression level of TLR2 in group A to E was 0.35±0.05, 0.30±0.03, 0.32±0.04, 0.30±0.02 and 0.29±0.03, respectively;the expression level of TLR4 in group A to E was 0.48±0.05, 0.34±0.03, 0.36±0.03, 0.37±0.04 and 0.35±0.02, respectively;the expression level of NF-κB p65 in group A to E was 0.43±0.03, 0.29±0.03, 0.35±0.02, 0.32±0.02 and 0.30±0.02, respectively. The differences in NEC morbidity, intestinal injury score, and the expression levels of TLR4, TLR2 and NF-κB p65 among the five groups were all statistically significant (χ2, H or F=23.863, 70.290, 8.803, 38.599 and 75.076, respectively, all P<0.05). The values in the NEC model group were all significantly higher than those in the other four groups (all P<0.05). The morbidity of NEC in the Biifdobacterium treatment group compared with the three control groups was not significantly different (all P > 0.05). The intestinal injury score in the Bifidobacterium treatment group was significantly higher than that in the Bifidobacterium control group and the breastfeeding control group (both P < 0.01), but was not significantly different to that in the artificial feeding control group (P > 0.05). The expression levels of TLR4 and NF-κB p65 in the Biifdobacterium treatment group were significantly lower than those in the artificial feeding control group and the Biifdobacterium control group (all P < 0.05), and were not significantly different to those in the breastfeeding control group (P>0.05). The expression level of TLR2 in the Biifdobacterium treatment group compared with the three control groups was not significantly different (all P > 0.05). Conclusions Biifdobacterium may inhibit pathogenic bacteria or regulate the negative feedback of TLR2 to reduce the expression of TLR2 and TLR4 in intestinal mucosa cells, inhibit the NF-κB pathway, attenuate the inflammatory reaction, and play a role in the prevention and control of NEC.

Through scale-up cultivation of Eriobotrya japonica suspension cells using WAVE bioreactor, the cell growth and ursolic acid (UA) accumulation were studied. The comparison test was carried out in the flask and the reactor with cell dry weight (DW) and UA content as evaluation indexes. The culture medium, DW and UA content were compared in 1 L and 5 L working volumes of bioreactor. The orthogonal test with main actors of inoculation amount, speed and angle of rotation was developed to find the optimal combination, in 1 L working volume of bioreactor. DW of the cell growth and the UA content in bioreactor were higher than those of the shaker by 105.5% and 27.65% respectively. In bioreactor, the dynamic changes of elements in the fluid culture, the dry weight of the cell growth and the UA content in 1 L and 5 L working volumes were similar. Inoculation of 80 g, rotational speed of 26 r · min(-1), and angle of 6 ° was the optimal combination, and the cell biomass of 19.01 g · L(-1) and the UA content of 27.750 mg · g(-1) were achieved after 100 h cultivation in 1 L working volume of bioreactor. WAVE Bioreactor is more suitable than flasks for the E. japonica cell suspension culture, and culture parameters can be achieved from 1 L to 5 L amplification.
Biomass ; Bioreactors ; Cell Culture Techniques ; instrumentation ; methods ; Culture Media ; chemistry ; metabolism ; Eriobotrya ; chemistry ; growth & development ; metabolism ; Triterpenes ; analysis ; metabolism

OBJECTIVETo explore the mechanism of the aging deformity of tear trough through the anatomic study of the tear trough region.

METHODS13 adult cadaveric heads (26 sides), including 9 male heads (18 sides) and 4 female heads (8 sides), aged 22-78 years old, were used. Anatomic study was performed around the orbital, especially tear trough region, with microsurgery instrument under microscope( x 10 times). The lower orbicularis retaining ligament was dissected and exposed. The anatomic location was recorded and photographed.

RESULTS(1) The anatomic layers of the tear trough region contains skin, subcutaneous tissue, orbicularis oculi muscle, periosteal membrane. There is no subcutaneous fat above the tear trough, while it exists below the tear trough, called malar fat pad. (2) There is a natural boundary between the septal and the orbital portions of the orbicularis oculi muscle of lower eyelid at surface of the orbital bone. The natural boundary, projected on the body surface corresponds to tear trough. The width of boundary is (2.06 +/- 0.15) mm on the vertical line through inner canthus and (3.25 +/- 0.12) mm on the vertical line through the lateral margin of the ala. The septal portion and the orbital portion of the orbicularis oculi muscle began to merge in (16.56 +/- 0.51) mm to inner canthus. (3) There is ligament attachment in the medial, upper and lower orbital and no ligament attachment in the lateral orbital. Orbicularis retaining ligament of lower eyelid is divided into two layers. (4) The medial of the upper layer of the orbicularis retaining ligament in lower eyelid originates from orbital margin and from preorbital walls laterally in (16.10 +/- 0.43) mm to the medial of lateral orbital margin, through orbicularis oculi muscle and ends at the skin. The lower layer of the orbicularis retaining ligament of lower eyelid originates from preorbital walls through orbicularis oculi muscle and its superficial fat, then ends at the skin.

CONCLUSIONSThe length of tear trough is (16.56 +/- 0.51) mm, the width of tear trough is (2.06 +/- 0.15) mm and (3.25 +/- 0.12) mm on the vertical line through inner canthus and the lateral margin of the ala nasi respectively. The main reason of the aging deformity of tear trough attributes to the increased distance between the upper and lower layers of the orbicularis retaining ligament in lower eyelid, which is caused by loose of the orbicularis retaining ligament and its underlying fat atrophy or decline.

Adult ; Aged ; Aging ; Cheek ; anatomy & histology ; Eyelids ; anatomy & histology ; Facial Muscles ; anatomy & histology ; Female ; Humans ; Lacrimal Apparatus ; anatomy & histology ; Male ; Middle Aged ; Young Adult

Objective To investigate the effect of interleukin 23 receptor (IL-23R) on T helper cell 17 (Th17) call-mediated immune response in mycobacterium tuberculosis (TB) infection,and to explore the role of IL-23R in the pathogenesis of pulmonary tuberculosis.Methods 21 active lung tuberculosis (ATB) patients were enrolled in Beijing chest hospital from July to October in 2015,21 cases of latent tuberculosis infection (LTBI) and 21 healthy Healthy Donors (HD) were selected from Beijing Changping center for tuberculosis control and prevention from May to July in 2015.The peripheral blood mononuclear cells (PBMCs) were isolated and cultured.The expression of IL-23R mRNA in PBMCs was detected,IL-23 and IL-17A levels in the supernatant of PBMCs were measured.The expression of IL-23R mRNA in different groups and the effect of IL-23R expression on IL-17A level were analyzed.Results The expression of IL-23R mRNA in ATB group was lower than that in LTBI group (Z =-2.528,P =0.011),and in ATB group was higher than that in HD group (Z =-3.849,P ＜ 0.001).The expression of IL-17A in ATB group was lower than that in LTB group (t =2.238,P =0.031),and ATB group was higher than that in HD group (t =4.733,P ＜ 0.001).There was no significant difference in IL-23 level between the three groups (F =0.432,P =0.651).IL-23R mRNA expression was positively correlated with IL-17A level (rs =0.438,P =0.047).Conclusions The expression level of IL-23R in mycobacterium tuberculosis infection can regulate the immune response mediated by Th17 cells,which may affect the susceptibility and infection outcome of pulmonary tuberculosis.

Objective The influenza A (H1N1) virus has the characteristic of strong infectiousness and variation. It can threaten the lives of patients. In this paper,we investigated the expression of programmed cell death molecule 5 (PDCD5) in peripheral blood of patients with influenza A (H1N1) and its correlation with the severity of disease. Methods The data of 104 patients with influenza A (H1N1) treated in Affiliated Hospital of Hebei University from January 2015 to December 2017 were analyzed retrospectively. The 104 patients were divided into the mild H1N1 group (n=78) and the severe H1N1 group (n=26). At the same time,104 healthy physical examination subjects were selected as control group. The blood routine,lymphocyte count and PDCD level were observed in three groups. Results The number of leukocytes,neutrophils and lymphocytes of the mild H1N1 group and severe H1N1 group were significantly lower than those of the control group (P<0.05). The number of leukocytes,neutrophils and lymphocytes of the severe H1N1 group were significantly lower than those of the mild H1N1 group (P<0.05). There was no significant difference in mononuclear cells between three groups (P>0.05). The levels of PDCD5 and lymphocyte apoptosis rate of the mild H1N1 group and severe H1N1 group were significantly higher than those of the control group (P<0.05) ,the severe H1N1 group was significantly higher than the mild H1N1 group (P<0.05). The total T cells,CD4+T cells and CD8+T cells of the mild H1N1 group and severe H1N1 group were significantly lower than those of the control group (P<0.05). The total T cells,CD4+T cells and CD8+T cells of the severe H1N1 group were significantly lower than those of the mild H1N1 group and con-trol group (P<0.05). The level of PDCD5 was positively correlated with the severity of disease and the rate of lymphocyte apoptosis (r=0.872,0.904,P<0.05),and negatively correlated with total T cells,CD4+T cells and CD8+T cells (r=-0.842,-0.805,-0.877,P<0.05). The sensitivity,specificity and area under the curve of PDCD5 to prediction of severe type H1N1 were 92.31%,97.25% and 0.941,respectively. Conclusion The level of peripheral blood PDCD5 in patients with influenza A (H1N1) virus in-fection is associated with the severity of the disease,and it can be considered as an important biomarker to predict severe influenza A (H1N1).

This study was aimed to investigate the effect of activated T cell on the ability of MSC to differentiate into osteoblasts. The activated T cells with MSCs were co-culture for 14 days, then the osteoblast formation was tested by alkaline phosphatase staining. Furthermore, the supernatant of activated T cell was added in culture system of MSCs, the expression of molecules related with immune regulation of activated T cells was detected by RT-PCR, so as to determine what kinds of cytokine displayed the important function in MSC differentiation. The result showed that activated T cell could promote differentiation of MSC into osteoblasts, and IL-1beta played an important role in the effect of activated T cells on MSCs, while TNF-alpha, TGF-beta1 were not. It is concluded that the activated T cells promote the differentiation of MSCs to osteoblasts. The interactive influence between MSCs and immune cells can be mediated through cytokines.
Cell Differentiation ; Cells, Cultured ; Coculture Techniques ; Culture Media, Conditioned ; Humans ; Interleukin-1beta ; biosynthesis ; Mesenchymal Stromal Cells ; cytology ; Osteoblasts ; cytology ; T-Lymphocytes ; metabolism

OBJECTIVETo investigate the role of calcium/calmodulin-dependent protein kinase II (CaMKII) in myocardial ischemia-reperfusion (IR) injury in isolated perfused rat heart and explore the underlying mechanisms.

METHODSAn ischemia-reperfusion (IR) model was prepared using isolated rat hearts perfused with Krebs-Henseleit solution were randomly divided into control group, 2.5 µmol/L KN-93 group, IR (induced by ischemia for 45 min followed by reperfusion for 120 min) group and KN-93+IR group. The myocardial performance was evaluated by assessing the left ventricular pressure. Lactate dehydrogenase (LDH) activity and cTnI content in the coronary flow and the infarct size were determined to evaluate the myocardial injury. The phosphorylation of CaMKII (p-CaMKII) and PLN (p-PLN) and oxidation of CaMKII (ox--CaMKII) were measured with Western blotting. The activity of mitochondrial superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were determined using ELISA.

RESULTSCompared with the control group, KN-93 treatment at 2.5 µmol/L produced no significant effects on cardiac function or performance in rat hearts without IR injury. Myocardial IR injury significantly decreased myocardial performance and mitochondrial SOD activity in the perfused hearts (P<0.01) and caused significantly increased infarct size, LDH activity, cTnI content, expressions of p-CaMKII, ox-CaMKII and p-PLN, and also increased mitochondrial MDA content (P<0.01). KN-93 treatment at 2.5 µmol/L administered before ischemia and before reperfusion markedly attenuated such changes induced by ischemia and reperfusion (P<0.01).

CONCLUSIONCaMKII participates in myocardial IR injury in isolated rat heart, and inhibiting CaMKII can alleviate myocardial injury by relieving mitochondrial oxidation stress.

OBJECTIVETo investigate the Effect of 2,3-butanedione monoxime (BDM) on calcium paradox-induced heart injury and its underlying mechanisms.

METHODSThirty-two adult male SD rats were randomized into 4 groups, namely the control group, BDM treatment control group, calcium paradox group, and BDM treatment group. Isolated Sprague Dawley male rat hearts underwent Langendorff perfusion and the left ventricular pressure (LVP) and left ventricular end-diastolic pressure (LVEDP) were monitored. Left ventricular developed pressure (LVDP) was calculated to evaluate the myocardial performance. Lactate dehydrogenase (LDH) content in the coronary flow was determined. Triphenyltetrazolium chloride staining was used to measure the infarct size, and myocardial cell apoptosis was tested with TUNEL method. Western blotting was used to determine the expression of cleaved caspase-3 and cytochrome c.

RESULTSCompared with the control group, BDM at 20 mmol/L had no effect on cardiac performance, cell death, apoptotic index or the content of LDH, cleaved caspase-3 and cytochrome c at the end of perfusion under control conditions (P>0.05). Calcium paradox treatment significantly decreased the cardiac function and the level of LVDP and induced a larger infarct size (P<0.01), an increased myocardial apoptosis index (P<0.01), and up-regulated expressions of cleaved caspase-3 and cytochrome c (P<0.01). BDM (20 mmol/L) significantly attenuated these effects induced by calcium paradox, and markedly down-regulated the levels of LVEDP and LDH (P<0.01), lowered myocardial apoptosis index, decreased the content of cleaved caspase-3 and cytochrome c (P<0.01), increased LVDP, and reduced the infarct size (P<0.01).

CONCLUSIONBDM suppresses cell apoptosis and contracture and improves heart function and cell survival in rat hearts exposed to calcium paradox, suggesting the value of BDM as an potential drug for myocardial ischemia reperfusion injur.

Animals ; Apoptosis ; Calcium ; adverse effects ; Caspase 3 ; metabolism ; Cytochromes c ; metabolism ; Diacetyl ; analogs & derivatives ; pharmacology ; Heart ; drug effects ; physiopathology ; In Vitro Techniques ; L-Lactate Dehydrogenase ; metabolism ; Male ; Myocardial Reperfusion Injury ; chemically induced ; drug therapy ; Rats ; Rats, Sprague-Dawley ; Ventricular Function, Left

OBJECTIVEto investigate the clinical characteristics in two families with early repolarization syndrome (ERS) and recurrent syncope.

METHODall family members including the probands were screened with routine clinical examination, electrocardiography, echocardiography, Holter recording, chest x-ray, head-up tilt test and blood biochemistry.

RESULTSthere was no clinical evidence of organic heart disease in all members from the two families. Proband 1 showed recurrent syncope, ERS and repeated torsade de pointes ventricular tachycardia and ventricular fibrillation were documented with resting ECG. ERS was detected in one brother, one nephew and one son from him and all were free of cardiac events including syncope, cardiac arrest and sudden cardiac death. Proband 2 showed recurrent syncope, ERS and ST segment arched upward elevation in V(1)-V(3) were documented by ECG. His father suffered sudden cardiac death at the age of 65 and asymptomatic ERS was detected in one of his nephew.

CONCLUSIONSERS is not always linked with benign clinical course and can sometimes lead to repeated syncope, torsade de pointes ventricular tachycardia and ventricular fibrillation. Pedigree research is of importance for ERS.

Adult ; Arrhythmias, Cardiac ; genetics ; Asian Continental Ancestry Group ; Humans ; Male ; Pedigree ; Recurrence ; Syncope ; genetics ; physiopathology ; Syndrome