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To improve the gas drainage effect of low-permeability coal seams, the influence of the hole arrangement on the static blasting effect was studied through single-hole, double-hole, and guiding-hole blasting tests. A stress-damage coupling model was established to reveal the evolution of the stress field and the distribution of the damage zone under different construction parameters, and the evolution law of the damage zone under a multi-hole arrangement was investigated. The following can be inferred from the research results. (1) The crack initiation of double holes depends on the stress superposition between blasting holes, whereas that of guiding holes depends on the free surface inside the coal body. The increase in borehole diameter and spacing reduction between boreholes could improve the static superposition breaking effect. (2) The relationship between the guiding hole, borehole diameter, and borehole spacing was revealed from the two aspects of the stress field and damage zone. The purpose is to strengthen the blasting effect. The drilling diameter and spacing are measured, and the guiding hole strengthens the blasting effect. At the measurement level, it should be analyzed from the two dimensions of time and stress. The time dimension accelerates the migration of the stress turning point, whereas the stress dimension realizes stress superposition and finally strengthens the static cracking effect. (3) The damage zone evolution of static blasting technology is influenced by expansion pressure, construction parameters, and elastic modulus. The increase in the expansion pressure caused the damage zone of the coal body and a decrease in the elastic modulus. Under the combined action of the expansion pressure and elastic modulus, the damage zone expanded and penetrated. The guiding borehole would not only have a guiding function but could also enhance the breaking effect. (4) In the simulation test scheme, the reasonable ratio of borehole spacing to borehole diameter is approximately 13 to 14, and the reasonable construction parameters are 113 mm of borehole diameter, 1.4 m of borehole spacing, and the layout of multi-hole-guiding hole. Static blasting technology can increase the distribution of the damaged areas of coal seams, realize pressure relief and permeability enhancement of coal seams, and improve the safe construction of coal mining.

A high-pressure and large-diameter extraction borehole is used in coal mines due to lack of understanding of the mechanism of negative pressure in the process of gas extraction, which will lead to problems such as poor gas extraction and collapse of the borehole. In order to solve these problems, the flow and pressure distribution in the process of variable mass flow of gas drainage borehole were studied based on factors such as orifice pressure, bore diameter, and bore flow. Firstly, we built a testing platform for variable mass flow pressure distribution and established a variable mass flow energy model and pressure distribution model. Secondly, the correlation between pressure distribution and orifice pressure, borehole diameter, and borehole flow in the process of variable mass flow was calculated by combining laboratory testing with numerical calculations. Finally, the results showed that with the increase in borehole length, pressure, and flow exhibited a downward trend during the variable mass flow of the borehole. Additionally, the pressure distribution in the borehole had a negative exponential relationship with borehole pressure and the diameter of the borehole. The pressure distribution in the borehole had a power-exponential relationship with the gas flow. These research results will provide a reference for the selection of reasonable parameters.

Psoriasis is a chronic skin disease characterized by abnormal keratinocyte proliferation and differentiation, inflammation, and angiogenesis. Overexpression of tribbles homolog3 (TRB3), which belongs to the tribbles family of pseudokinases, has been found in several human tumors and metabolic diseases, but its role in psoriasis has not been fully clarified. The aim of this study is to investigate the expression of TRB3 in psoriasis and explore its roles in the proliferation of keratinocytes. Twenty-four patients with psoriasis vulgaris were recruited for the study. Diagnosis of psoriasis was based on clinical and histologic examinations. Immunohistochemistry and real-time reverse transcription PCR (RT-PCR) were performed to determine protein and messenger RNA (mRNA) expression of TRB3 in psoriasis lesions. 5-Bromo-2-deoxyUridine (BrdU) incorporation assay were performed for cell proliferation. Cell cycle distribution was assessed by flow cytometry analysis. The levels of TRB3 is elevated in psoriatic lesions compared with psoriatic non-lesions. The HaCat cells expressed the TRB3 gene. We found TRB3 silencing to significantly inhibit HaCat cell proliferation. Furthermore, the specific knockdown of TRB3 slowed down the cell cycle at the gap 0/first gap phase. In conclusion, our data suggest that TRB3 is overexpressed in lesions of patients with psoriasis and may be involved in the abnormal proliferation of keratinocytes. Therefore, TRB3 may be a potential therapeutic target for psoriasis.

Through the establishment of contact element simulated the contact between sucker rod and oil pipe. The deformation of sucker rods in oil pipe that caused by the screw pump rotor eccentricity has been researched by the application of transient dynamics analysis. Results show that screw pump rotor eccentricity is one of the reasons which cause rod and oil pipe contact resulting in partial abrasion. Deformation of the sucker rods caused by the rotor eccentricity is mainly concentrated on the bottom of rods, so in order to mitigate partial abrasion, rod centralizer arrangement at the bottom of rods should be strengthened, or change the connection mode between the sucker rod and screw pump rotor to eliminate the effect of the sucker rod deformation caused by rotor eccentric motion.

Introduction With the advent of genetically engineered mice, it seems important to develop a mouse model of cavernous nerve injury (CNI). Aim To establish a mouse model of CNI induced either by nerve crushing or by neurectomy and to evaluate time-dependent derangements in penile hemodynamics in vivo and subsequent histologic alterations in the cavernous tissue. Methods Twelve-week-old C57BL/6J mice were divided into 4 groups (N = 36 per group): control, sham operation, bilateral cavernous nerve crush, and bilateral cavernous neurectomy group. Main Outcome Measures Three days and 1, 2, 4, 8, and 12 weeks after CNI, erectile function was measured by electrical stimulation of the cavernous nerve. The penis was then harvested and TUNEL was performed. Immunohistochemical analysis was performed assaying for caspase-3, transforming growth factor-β1 (TGF-β1), phospho-Smad2, PECAM-1, factor VIII, and smooth muscle α-actin. The numbers of apoptotic cells and phospho-Smad2-immunopositive cells in endothelial cells or smooth muscle cells were counted. Results Erectile function was significantly less in the cavernous nerve crushing and neurectomy groups than in the control or sham group. This difference was observed at the earliest time point assayed (day 3) and persisted up to 4 weeks after nerve crushing and to 12 weeks after neurectomy. The apoptotic index peaked at 1 or 2 weeks after CNI and decreased thereafter. Cavernous TGF-β1 and phospho-Smad expression was also increased after CNI. The numbers of apoptotic cells and phospho-Smad2-immunopositive cells in cavernous endothelial cells and smooth muscle cells were significantly greater in the cavernous nerve crush and cavernous neurectomy groups than in the control or sham group. Conclusion The mouse is a useful model for studying pathophysiologic mechanisms involved in erectile dysfunction after CNI. Early intervention to prevent apoptosis in smooth muscle cells and endothelial cells or to inhibit cavernous tissue fibrosis is required to restore erectile function. Jin H-R, Chung YG, Kim WJ, Zhang LW, Piao S, Tuvshintur B, Yin GN, Shin SH, Tumurbaatar M, Han J-Y, Ryu J-K, and Suh J-K. A mouse model of cavernous nerve injury-induced erectile dysfunction: Functional and morphological characterization of the corpus cavernosum.

Introduction Transforming growth factor-β1 (TGF-β1) has been known to play a crucial role in the pathogenesis of Peyronie's disease (PD). Aim The aim of this paper was to investigate the therapeutic effect of IN-1130, a novel small molecule inhibitor of activin receptor-like kinase (ALK)5, a type I receptor of TGF-β, in an animal model of PD. Methods PD was induced in rats through repeated injections of adenovirus expressing TGF-β1 (days 0, 3, and 6; 1 × 10 10 particles/0.1 mL, respectively) into the tunica albuginea. The rats were divided into five groups (N = 10 per group): group 1, age-matched controls without treatment; group 2, age-matched controls receiving repeated injections of IN-1130 (days 30 and 37; 5 mg/kg in 0.1 mL saline, respectively); group 3, PD rats without treatment; group 4, PD rats receiving repeated injections of saline (days 30 and 37; 0.1 mL, respectively); group 5, PD rats receiving repeated injections of IN-1130 (days 30 and 37; 5 mg/kg in 0.1 mL saline, respectively) into the lesion. Main Outcome Measures Penile curvature was evaluated by use of an artificial erection test at day 45, and the penis was then harvested for histologic examination. Collagen in the plaque was quantitatively assessed by hydroxyproline determination. Results IN-1130 induced significant regression of fibrotic plaque through reduced infiltration of inflammatory cells, reduced transnuclear expression of phospho-Smad2/phospho-Smad3, reduced hydroxyproline content, and reduced cartilage content and restoration of elastin fibers in the fibrotic plaque of PD rats, which was accompanied by the correction of penile curvature. Conclusion Antagonizing TGF-β signaling through the use of ALK5 inhibitors may represent an exciting new therapeutic strategy for the future treatment of PD. Ryu J-K, Piao S, Shin H-Y, Choi MJ, Zhang LW, Jin H-R, Kim WJ, Han J-Y, Hong SS, Park SH, Lee S-J, Kim I-H, Lee CR, Kim D-K, Mamura M, Kim S-J, and Suh J-K. IN-1130, a novel transforming growth factor-β type I receptor kinase (activin receptor-like kinase 5) inhibitor, promotes regression of fibrotic plaque and corrects penile curvature in a rat model of Peyronie's disease. J Sex Med 2009;6:1284–1296.

Introduction It has been suggested that transforming growth factor‐β1 (TGF‐β1) plays an important role in the pathogenesis of diabetes‐induced erectile dysfunction. Aim To investigate the expression and activity of Smad transcriptional factors, the key molecules for the initiation of TGF‐β‐mediated fibrosis, in the penis of streptozotocin (STZ)‐induced diabetic rats. Methods Fifty‐two 8‐week‐old Sprague–Dawley rats were used and divided into control and diabetic groups. Diabetes was induced by an intravenous injection of STZ. Main Outcome Measures Eight weeks later, erectile function was measured by electrical stimulation of the cavernous nerve (N = 12 per group). The penis was harvested and stained with Masson trichrome or antibody to TGF‐β1, phospho‐Smad2 (P‐Smad2), smooth muscle α‐actin, and factor VIII (N = 12 per group). Penis specimens from a separate group of animals were used for TGF‐β1 enzyme‐linked immunosorbent assay (ELISA), P‐Smad2/Smad2, phospho‐Smad3 (P‐Smad3)/Smad3, fibronectin, collagen I, and collagen IV western blot, or hydroxyproline determination. Results Erectile function was significantly reduced in diabetic rats compared with that in controls. The expression of TGF‐β1, P‐Smad2, and P‐Smad3 protein evaluated by ELISA or western blot was higher in diabetic rats than in controls. Compared with that in control rats, P‐Smad2 expression was higher mainly in smooth muscle cells and fibroblasts of diabetic rats, whereas no significant differences were noted in endothelial cells or in the dorsal nerve bundle. Cavernous smooth muscle and endothelial cell contents were lower in diabetic rats than in controls. Cavernous fibronectin, collagen IV, and hydroxyproline content was significantly higher in diabetic rats than in controls. Conclusion Upregulation of TGF‐β1 and activation of the Smad signaling pathway in the penis of diabetic rats might play important roles in diabetes‐induced structural changes and deterioration of erectile function. Zhang LW, Piao S, Choi MJ, Shin H‐Y, Jin H‐R, Kim WJ, Song SU, Han J‐Y, Park SH, Mamura M, Kim S‐J, Ryu J‐K, and Suh J‐K. Role of increased penile expression of transforming growth factor‐β1 and activation of the Smad signaling pathway in erectile dysfunction in streptozotocin‐induced diabetic rats. J Sex Med 2008;5:2318–2329.

Background. Renal transplantation is currently the prevalent therapy for most patients with end-stage renal disease. No clinical markers for such rejection have been universally accepted. We aimed to investigate the possibility of use of human leukocyte antigen (HLA) class I (ABC) on peripheral blood CD3+/CD8+ T lymphocytes as a marker of acute rejection. Methods. For recipients undergoing renal transplantation from September 2007 to November 2008, peripheral blood samples were obtained pretransplantation and at days 3 and 7 posttransplantation when the patients were still hospitalized and at weeks 2 and 3 and months 1, 2, 3, and 6 posttransplantation. For patients with fever, lumbodynia, gross hematuria, or oliguria after transplantation, blood samples were collected immediately before and at days 3 and 7 after the administration of anti-inflammatory regents. The level of HLA class I (ABC) on peripheral-blood CD3+/CD8+ T lymphocytes was measured on flow cytometry. Results. For the 79 transplant recipients, the level of HLA class I (ABC) on peripheral-blood CD3+/CD8+ T lymphocytes was consistently elevated during the first 3 weeks after transplantation, declined gradually to pretransplantation levels, then tapered off and remained stable. Patients experiencing acute rejection (AR) or not after transplantation did not differ in level of HLA class I (ABC) up to 6-month follow-up, except at days 14 and 21 after transplantation, when the level was higher for patients experiencing AR (P Conclusions. Upregulation of HLA class I (ABC) on peripheral-blood CD3+/CD8+ T lymphocytes could be used as an accurate and reliable predictor of AR after renal transplantation.

Introduction Endothelial cell-to-cell junctions are crucial for vascular formation, networking, and remodeling of blood vessels as well as for inducing and integrating intracellular signals. Aim We investigated the differential expression and distribution of endothelial cell-to-cell junction proteins in the penis of mice with hypercholesterolemia-induced erectile dysfunction. Methods Two-month-old C57BL/6J mice were fed a diet containing 4% cholesterol and 1% cholic acid, and age-matched control animals were fed a normal diet, for 3 months. We performed dual priming oligonucleotide (DPO)-based multiplex polymerase chain reaction (PCR) (Seegene, Seoul, Korea) to screen the differential gene expression of 21 endothelial cell-to-cell junctions. Main Outcome Measures At 5 months, erectile function was measured by electrical stimulation of the cavernous nerve, and the penis was harvested and stained with antibody to claudin-5, vascular endothelial (VE)-cadherin, and platelet/endothelial cell adhesion molecule (PECAM)-1 (N = 8 per group). Cavernous specimens from a separate group of animals were used for claudin-5, VE-cadherin, and PECAM-1 reverse transcriptase-PCR and Western blot analysis. Results Erectile function was significantly lower in hypercholesterolemic mice than in controls. DPO-based multiplex PCR revealed a profound decrease in the gene expression of endothelium-specific cell-to-cell junction proteins, including claudin-5, VE-cadherin, and PECAM-1, in hypercholesterolemic mice compared with that in controls. The expression of claudin-5, VE-cadherin, and PECAM-1 protein evaluated by Western blot or immunohistochemistry was significantly lower in hypercholesterolemic mice than in controls. These endothelial cell-to-cell junction proteins were more sparsely distributed in the endothelium of cavernous sinusoids than in the endothelium of cavernous artery and dorsal blood vessels. Conclusion Down-regulation of the endothelial cell-to-cell junctions and decreased endothelial content in the corpus cavernosum might play a major role in the deterioration of erectile function in hypercholesterolemic mice. Ryu J-K, Zhang LW, Jin H-R, Piao S, Choi MJ, Tuvshintur B, Tumurbaatar M, Shin SH, Han J-Y, Kim WJ, and Suh J-K. Derangements in endothelial cell-to-cell junctions involved in the pathogenesis of hypercholesterolemia-induced erectile dysfunction. J Sex Med 2009;6:1893–1907.

Introduction The application of gene therapy for a nonlife-threatening disease, such as erectile dysfunction (ED), requires a higher safety level and more efficacious systems for gene transfer. Aim To establish a novel technique for gene expression in a rat model of hypercholesterolemic ED that uses the RTP801 promoter, a hypoxia-inducible promoter. Methods Two-month-old male Sprague–Dawley rats were fed a diet containing 4% cholesterol and 1% cholic acid, and age-matched control animals were fed a normal diet, for 3 months. Main Outcome Measures Cavernous expression of hypoxia-inducible factor (HIF)-1α was evaluated by Western blot. After intracavernous injection of pSV-Luc or pRTP801-Luc, gene expression was evaluated by luciferase assay, and the gene expression area was evaluated by immunohistochemistry. Results HIF-1α was up-regulated in the corpus cavernosum of hypercholesterolemic rats. Although pSV-Luc did not induce gene expression in either the control or the cholesterol group, pRTP801-Luc significantly induced gene expression in the cholesterol group and resulted in higher luciferase activity than did pSV-Luc up to 14 days after injection. Immunohistochemistry showed that the gene expression area was also greater in the pRTP801-Luc group than in the pSV-Luc group, but the difference was not as great as that in luciferase activity. This suggests that pRTP801-Luc exerts its effect mainly by inducing promoter activity under hypoxia, not by increasing the number of transfected cells. Conclusion The RTP801 promoter-driven gene expression system increased gene expression in the corpus cavernosum tissue of rats with cholesterol-induced ED. This may be a useful system for the development of gene therapy in vasculogenic ED. Lee M, Ryu J-K, Piao S, Choi MJ, Kim HA, Zhang L-W, Shin H-Y, Jung HI, Kim I-H, Kim SW, and Suh J-K. Efficient gene expression system using the RTP801 promoter in the corpus cavernosum of high-cholesterol diet-induced erectile dysfunction rats for gene therapy.