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B1型胸腺瘤被认为是一种生物学行为较良善的B型胸腺瘤，通常认为其复发或转移发生于原发病变的中、晚期。该文报道1例原发于纵隔的B1型胸腺瘤，原发病程分期较早，但转移隐匿，不易发觉，其转移灶表现为巨大肝脏占位和多发性肺部占位。提示部分B1型胸腺瘤具有在病变早期复发、远处转移的恶性生物学行为，对这一部分病变的甄别可借助免疫组织化学染色p53和BCOR蛋白的阳性表达。.

Periventricular leukomalacia (PVL) is one of the foremost neurological conditions leading to long-term abnormalities in premature infants. Since it is difficult to prevent initiation of this damage in utero, promoting the innate regenerative potential of the brain after birth may provide a more feasible, prospective therapy for PVL. Treatment with UDP-glucose (UDPG), an endogenous agonist of G protein-coupled receptor 17 (GPR17) that may enhance endogenous self-repair potentiality, glial cell line-derived neurotrophic factor (GDNF), a neurotrophic factor associated with the growth and survival of nerve cells, and memantine, a noncompetitive antagonist of N-methyl-d-aspartate (NMDA) receptors that block ischemia-induced glutamate signal transduction, has been reported to achieve functional, neurological improvement in neonatal rats with PVL. The aim of the present study was to further explore whether UDPG, GDNF and/or memantine could promote corresponding self-repair of the subventricular zone (SVZ) and white matter (WM) in neonatal rats with ischemia-induced PVL. SVZ or WM tissue samples and cultured glial progenitor cells derived from a 5 day-old neonatal rat model of PVL were utilized for studying response to UDPG, GDNF and memantine in vivo and in vitro, respectively. Labeling with 5'-bromo-2'-deoxyuridine and immunofluorescent cell lineage markers after hypoxia-ischemia or oxygen-glucose deprivation (OGD) revealed that UDPG, GDNF and memantine each significantly increased glial progenitor cells and preoligodendrocytes (preOLs), as well as more differentiated immature and mature oligodendrocyte (OL), in both the SVZ and WM in vivo or in vitro. SVZ and WM glial cell apoptosis was also significantly reduced by UDPG, GDNF or memantine, both in vivo and in vitro. These results indicated that UDPG, GDNF or memantine may promote endogenous self-repair by stimulating proliferation of glial progenitor cells derived from both the SVZ and WM, activating their differentiation into more mature OLs, and raising the survival rate of these newly generated glial cells in neonatal rats with ischemic PVL.

Fatigue failure of a high manganese steel crossing is related to its internal crack initiation and growth, which is affected significantly by the magnitude and distribution pattern of contact stress and residual stress in the crossing. Considering the actual service conditions of a crossing and the accuracy requirement for numerical calculation, a whole model of wheel/crossing/ties and a partial model of wheel/crossing are established using elastic-plastic finite element method. The distributions of contact stress fields and residual stress fields due to wheel contact loading are studied. The effect of train speed on the residual stress in the nose rail is discussed. The contact stress field shows regular contours in the cross-section of nose rail and decreases remarkably with increasing distance of the wheel-crossing contact position. The maximum contact stress is located at the contact surface between wheel and crossing. The maximum residual stress is located at a position of 1.5-2.0 mm below the surface of the nose rail, rather than at the contact surface of wheel and crossing. In a failed high manganese steel crossing, the dense cracks mainly were observed neither at the position of maximum contact stress (the contact surface between the wheel and the crossing), nor at the position of maximum residual stress (1.5-2.0 mm below the surface of the nose rail), but around the depth of 0.8-1.0 mm from the worn surface, which is between the position of maximum contact stress and the position of maximum residual stress. It indicates that the combined effects of the maximum contact stress and the maximum residual stress play important roles in fatigue crack initiation in the nose rail. The size of high residual stress region increases with the increase of the train speed. The maximum residual stress in the nose rail increases remarkably with the increase of the train speed.

In this paper, we use the homotopy analysis method (HAM) to solve the homoclinic orbit in an autonomous buckled thin plate system. Comparisons are made between the results of the proposed method and exact solutions. The results show that the HAM is an attractive and effective technique of analytic approximation for a homoclinic orbit. The proof of convergence theorems for the present method is elucidated as well. Besides, it leaves ample rooms for further investigating a homoclinic orbit that cannot be resorted to exact treatment.

Osteoarthritis (OA) is the leading cause of joint pain and disability in middle-aged and elderly patients, and is characterized by progressive loss of articular cartilage that eventually leads to a complex process involving degradation of various components of the cartilage matrix, chief among them are the cartilage-specific type II collagen (CII) and aggrecan. While the loss of aggrecan is thought to be an early and reversible process, degradation of CII is considered to be irreversible and a key step in the loss of structural and functional integrity of cartilage. Among the various matrix metalloproteinases (MMPs), MMP-13 is specifically expressed in the cartilage of human OA patients and is not present in normal adult cartilage. It is the major collagenase in OA cartilage and has the highest activity against CII. However, the clinical utility of broad-spectrum MMP inhibitors developed for treatment of OA has been restricted by dose- and duration-dependent musculoskeletal side effects in humans. Consequently, selectively inhibiting the MMP-13 would seem to be an attractive therapeutic objective. This review mainly focuses on selective MMP-13 inhibitors development in terms of OA since the late 90s, in terms of synthetic compounds of low molecular mass incorporating specific zinc-binding groups, non-zinc-binding groups. In addition, dual inhibitors of MMP-13 and aggrecanase are also reviewed. Special emphasis is placed on logistic concerns for lead compound search as well as the structure-activity relationship (SAR) in this field. Through these methods, new hope is emerging for the treatment of OA through selective inhibition of MMP-13.

In this study, atom probe tomography was employed to investigate atomic-scale element distributions in an electroplated nanocrystalline Ni alloy. Quantitative characterization evidences that weak yet detectable grain boundary segregations of carbon and cobalt occur during low-temperature electroplating. Nanoindentation measurements suggest that the hardness of the alloy is ~1 GPa higher than that of the nanocrystalline pure Ni with the same grain size. Classical solid solution strengthening cannot completely account for the hardness increment and hence the grain boundary segregations appear to play an important role in the strength improvement.

To evaluate the ability of epristeride to inhibit the prostatic glandular regrowth.Normal rats were castrated. Testosterone was injected to induce the regrowth of glandular cells. HE staining was performed. The height of the glandular epithelium and the acinar luminal areas were determined, and dihydrotestosterone (DHT) was detected by immunohistochemistry.Both the height and the acinar luminal areas were reduced by 48 % and 55 % in epristeride-treated group compared with control group respectively. The staining of DHT was comparatively strong in the control group. After 30-d of treatment, it turned much weaker.The regrowth of glandular cells was inhibited by epristeride via declining of the DHT concentration in the rat prostate.

To study molecular mechanism of epristeride in the treatment of benign prostatic hyperplasia and discuss the possibility of using prostate acid phosphatase (ACP) as a marker of the atrophy of prostatic gland in vivo.Morphological changes in cells were observed by light microscope. TdT-mediated dUTP-biotin nick end labeling (TUNEL) technique and agarose gel electrophoresis were performed to detect the nucleosomal DNA fragmentation. The activity of pACP was also assayed.Apoptosis occurred in both castration- and epristeride- treatment group. Both the degree and extent of apoptosis are much larger in the group of castration than that of epristeride-treated group. Both epristeride and castration decreased the prostate wet weight and DNA content but increased the prostate DNA concentration. Maximal or near maximal decreases were seen by d 10 in both groups. The activity of ACP was decreased by both castration and epristeride treatment. Changes in the ACP activity during treatment were coincide with other changes such as the prostate wet weight and DNA content.Apoptosis induced by epristeride was one of mechanisms in the treatment of benign prostatic hyperplasia and the activity of ACP could be used as a marker of prostate atrophy.

To study the effect of nomegestrol acetate, a new synthetic progesterone on granulosa cells' viability and steroidogenesis function.Granulosa cells were cultured in McCoy's 5A medium. Trypan blue stain was used to measure viable cells. FSH and testosterone were added to stimulate the steroid secretion. Specific RIA assay was used to evaluate the estrogen and progesterone secretion respectively.IC50 of nomegestrol acetate to damage cells is 6.85 mg/L (95 % confidence limits 5.36-8.75 mg/L). Nomegestrol acetate 0.45, 0.9, and 1.8 mg/L greatly inhibited the estrogen secretion from granulosa cells by 7.6 %, 12.5 %, 28.3 % in the presence of testosterone 0.5 micromol/L and FSH 10 U/L without affecting the number of viable cells. The secretion of progesteron were markedly decreased by 44.5 %, 53.3 %, and 62.0 % concurrently.Nomegestrol acetate directly inhibited the steroidogenesis of granulosa cells.

This paper concentrates solely on the effect of end bend airfoil on performance of an axial flow compressor. The purpose is to reduce flow loss in the region of endwall boundary layer and to enlarge surge margin of an axial flow compressor by employing end bend airfoil on the stator blades in the last stages of the compressor. The experimental results show that surge margin is increased by 4.9–5.2 percent, efficiency by 2.6–3.2 percent at operational speed n=1.0–1.1.Copyright © 1985 by ASME