The currently used heart valve prosthesis are still far from the ideal one in anticoagulation and longevity. The construction of tissue engineering heart valve leaflets are carried out recently. This article reviews the progress of tissue engineering heart valve leaflets in implanting materials, seeded cells, animal experiment and basic research. It also discusses the benefits and feasibility of tissue engineering heart valve leaflets.

Adenocarcinoma, Follicular ; metabolism ; pathology ; Adenoma, Chromophobe ; metabolism ; pathology ; Adenoma, Oxyphilic ; metabolism ; pathology ; Angiomyoma ; metabolism ; pathology ; Biomarkers, Tumor ; metabolism ; Carcinoma, Papillary ; metabolism ; pathology ; Carcinoma, Renal Cell ; classification ; metabolism ; pathology ; ultrastructure ; Diagnosis, Differential ; Humans ; Kidney Neoplasms ; classification ; metabolism ; pathology ; ultrastructure ; Thyroid Neoplasms ; metabolism ; pathology

OBJECTIVETo explore the correlation of the gene polymorphisms of Toll-like receptor 2 ( TLR2) and TLR4 with the susceptibility and recurrence of condyloma acuminatum (CA).

METHODSUsing Snapshot, we detected the gene polymorphisms of TLR2 597(T/C), 1350(T/C), 15607(A/G), and 2258(G/A) and TLR4 896(A/G) and 1196(C/T) in the peripheral blood of 140 CA patients and 105 HPV-negative controls. We made comparisons between the CA patients and controls as well as between the cases of recurrent CA and those of non-recurrence at 6 months after treatment.

RESULTSThere were 72, 48, and 20 cases of genotype TT, TC, and CC of TLR2 597 (T/C), respectively, in the CA patients, as compared with 71, 31, and 3 cases in the controls. The gene frequency of mutant C was 31. 43% in the patients, significantly higher than 17.62% in the controls (χ2 = 12.04, P < 0.01), and it was 38.68% in the recurrent cases, remarkably higher than 27.01% in the non-recurrent cases (χ2 = 4.16, P < 0.05). There were 74, 49, and 17 cases of genotype TT, TC, and CC of TLR2 1350( T/C), respectively, in the CA patients, as compared with 73, 29, and 3 cases in the controls. The gene frequency of mutant C was 29. 64% in the patients, significantly higher than 16. 67% in the controls (χ2 =11.05, P < 0.01), and it was 36.79% in the recurrent cases, markedly higher than 25. 29% in the non-recurrent cases (χ2 = 4.18, P < 0.05). There were 44, 66, and 30 cases of genotype AA, AG, and GG of TLR2 15607(A/G), respectively, in the CA patients, as compared with 26, 58, and 21 cases in the controls. There was no significant difference in the gene frequencies of mutant G between the two groups (χ2 = 0.33, P > 0.05). No mutant genes of TLR2 2508 (G/A) or TLR4 896(A/G) and 1196(C/ T) were detected in either the CA patients or the controls. Linkage disequilibrium analysis showed a tight linkage between TLR2 597 (T/C) and 1350(T/C) (D' = 1, r2 = 0.93).

CONCLUSIONTLR2 597(T/C) is tightly linked to 1350(T/C), which is correlated with both the susceptibility and the recurrence of condyloma acuminatum.

Aged ; Case-Control Studies ; Condylomata Acuminata ; genetics ; Gene Frequency ; Genetic Linkage ; Genetic Predisposition to Disease ; Genotype ; Humans ; Polymorphism, Genetic ; Recurrence ; Toll-Like Receptor 2 ; genetics ; Toll-Like Receptor 4 ; genetics

Hamartoma ; pathology ; Humans ; Lung Neoplasms ; pathology

Carcinoma in Situ ; epidemiology ; etiology ; pathology ; Carcinoma, Squamous Cell ; pathology ; surgery ; Disease Progression ; Female ; Humans ; Lichen Sclerosus et Atrophicus ; epidemiology ; etiology ; pathology ; Prevalence ; Vulvar Neoplasms ; epidemiology ; etiology ; pathology

OBJECTIVETo investigate the effect of siRNA silencing the role of C-Jun N-terminal Kinase (JNK) gene in excessive endoplasmic reticulum stress on lung ischemia/reperfusion injury.

METHODSMouse model of pulmonary ischemia reperfusion injury (PIRI) in situ was established with unilateral lung in vivo. Seventy experimental mice were randomly allocated into seven groups (n = 10): Sham group (Sham group), ischemia reperfusion group (I/R), PBS+ Lipofectamine2000TM transfection reagent group (I/R + PBS+ Lipo group), negative control group (I/R+ SCR group), JNK-siRNA group (I/R + siRNA(JNK1), siRNA(JNK2), siRNA(JNK3)). Mice were euthanized after experimental time out, and left lung tissue was extracted. Wet/dry lung weight ratio (W/D) and total lung water content (TLW) were tested. Light microscope, alveolar damage quantitative evaluation index (IQA) and electron microscope were observed. The expression levels of JNK and glucose regulatex protein(GRP78) were detected by RT-PCR and Western blot. Apoptosis of lung tissue was determined by TUNEL.

RESULTSCompared with Sham group, all indicators above of I/R + PBS + Lipo group and I/R + SCR group were significantly increased (P < 0.01), and compared with I/R group, those indicators of the three groups all had no notable difference; those indicators were not statistically different between I/R + PBS + Lipo group and I/R + SCR group, and compared to the three groups, the above indicators in JNK-siRNA group were lower (P < 0.05, P < 0.01) except that the expression levels of GRP78 was not statistically different.

CONCLUSIONI/R induces excessive ERS in lung tissue, in which JNK pathway participates in apoptosis, leading to lung tissue injury.

Animals ; Apoptosis ; Endoplasmic Reticulum Stress ; Heat-Shock Proteins ; metabolism ; JNK Mitogen-Activated Protein Kinases ; genetics ; Lung ; physiopathology ; Lung Injury ; genetics ; MAP Kinase Signaling System ; Mice ; RNA, Small Interfering ; Reperfusion Injury ; genetics

Adult ; Benzene ; poisoning ; Chronic Disease ; Female ; Humans ; Occupational Diseases ; diagnosis

BACKGROUND: Autologous stem cell transplantation (autoSCT) can extend remission of mantle cell lymphoma (MCL), but the management of subsequent relapse is challenging. METHODS: We examined consecutive patients with MCL who underwent autoSCT at Veterans Affairs Puget Sound Health Care System between 2009 and 2017 (N=37). RESULTS: Ten patients experienced disease progression after autoSCT and were included in this analysis. Median progression free survival after autoSCT was 1.8 years (range, 0.3–7.1) and median overall survival after progression was only 0.7 years (range, 0.1 to not reached). The 3 patients who survived more than 1 year after progression were treated with ibrutinib. CONCLUSION Our findings suggest that ibrutinib can achieve relatively prolonged control of MCL progressing after autoSCT.

OBJECTIVETo investigate the role of voltage-gated potassium channels in the acute hypoxic pulmonary vasoconstriction.

METHODSThirty Wistar rats were divided into two groups, namely the normoxic group and hypoxic group. The single smooth muscle cell was obtained from the pulmonary artery of Wistar rats with acute enzymatic digestion method. The conventional whole-cell patch clamp technique was used to record the resting membrane potential(Em) and the potassium currents of voltage-gated potassium channel (IKv) in rat pulmonary arterial smooth muscle cells(PASMC). Intracellular application of Kv1.2, Kv1.3, Kv1.5, and Kv2.1 antibodiesè1:125éwas conducted through the whole-cell patch clamp system.

RESULTSEm of PASMC was depolarized in hypoxia compared with that of control cells. The mixture of Kv1.2, Kv1.3, Kv1.5, and Kv2.1 antibodiesè1:125é depolarized Em and inhibited Ikv in PASMC from normoxic rat,whereas the mixture of Kv1.2, Kv1.3, Kv1.5, Kv2.1 antibodiesè1:125éhad no effects on Ikv and Em in hypoxic rats.

CONCLUSIONKv1.2, Kv1.3, Kv1.5, Kv2.1 might be oxygen sensitive potassium channels which mediated acute hypoxic pulmonary vasoconstriction.

Animals ; Hypoxia ; physiopathology ; Membrane Potentials ; drug effects ; Muscle, Smooth, Vascular ; physiopathology ; Patch-Clamp Techniques ; Potassium Channels, Voltage-Gated ; physiology ; Pulmonary Artery ; pathology ; physiology ; Rats ; Rats, Wistar ; Vasoconstriction ; physiology

OBJECTIVETo evaluate the effects of treadmill running exercise of different intensity on early repair of full-thickness defects on the patellofemoral articular surface and the changes in the expressions of matrix metalloproteinase-3 (MMP-3) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in SD rats.

METHODSTwenty-four male SD rats with full-thickness defects on the patellofemoral articular surface were randomly assigned into sedentary control (SED) group and low-, moderate- and high-intensity running groups (LIR, MIR, and HIR groups, respectively). The running groups were trained on treadmill for 6 consecutive weeks. Blood samples were collected to detect serum MMP-3 and TIMP-1 levels using ELISA before and after the experiment, and the femoral trochlea were collected to assess tissue repair by gross appearance scoring and O Driscoll histological scoring with Safranine O-Fast Green staining and Toluidine blue staining.

RESULTSIn rats in SED group, the defect was filled with hyaline articular cartilage-like tissues, as compared to fibrous tissues in LIR and MIR groups and subchondral bone damage in HIR group. The SED group scored the highest and HIR group the lowest among the 4 groups in gross appearance scoring and O Driscoll histological scoring. No significant differences were found in MMP-3 or TIMP-1 levels among the groups before training (P>0.05), but after 6 weeks of training, serum MMP-3 and TIMP-1 levels differed significantly among the 4 groups (P<0.05), and all the 3 running groups had a significantly higher MMP-3 level than the control group (P<0.05). After the 6-week training, TIMP-1/MMP-3 ratio was significantly higher in SED group than in the 3 running groups, and was the lowest in HIR group.

CONCLUSIONBoth low- and moderate-intensity exercise failed to promote resurfacing of full-thickness cartilage defects on the patellofemoral articular surface in rats, and high-intensity exercise even induces subchondral bone damage. The expression of MMP-3 and TIMP-1 is related to exercise, and the TIMP-1/MMP-3 ratio reflects the extent of tissue repair.

Animals ; Cartilage, Articular ; metabolism ; pathology ; Male ; Matrix Metalloproteinase 1 ; metabolism ; Matrix Metalloproteinase 3 ; metabolism ; Physical Conditioning, Animal ; Rats ; Rats, Sprague-Dawley ; Tissue Inhibitor of Metalloproteinase-1 ; metabolism ; Wound Healing