Decorin is the predominant proteoglycan synthesized within the meniscus from young individuals fungus gnats on orchids trusted 10 mg lotrisone, whereas the relative proportion of aggrecan synthesis increases with age. The meniscus was defined originally as a fibrocartilage, primarily based on the rounded or oval form of most of the cells and the fibrous microscopic look of the extra-cellular matrix. Based on molecular and spatial standards, three distinct populations of cells are recognized within the meniscus of the knee joint132: 1. The fibroblast-like cells lack a pericellular matrix and are positioned within the outer portion of the meniscus. They are distinguished by lengthy, thin, branching cytoplasmic projections that stain for vimentin. They make contact with other cells in different regions by way of connexin 43�containing gap junctions. The presence of two centrosomes, one associated with a main cilium, suggests a sensory, rather than motile, operate that could allow the cells to reply to circumferential tensile hundreds rather than compressive hundreds. The superficial zone cells have a attribute fusiform form with no cytoplasmic projections. Cell lineage tracing and gene profiling studies in mouse embryos have offered perception into the complexity of the meniscus and how it was formed. Lubrication by synovial fluid provides frictionless movement of the articulating cartilage surfaces. Chondrocytes (see Chapter 3) are the only cellular component of grownup hyaline articular cartilage and are answerable for synthesizing and maintaining the highly specialized cartilage matrix macromolecules. The cartilage extra-cellular matrix is composed of an in depth network of collagen fibrils, which confers tensile energy, and an interlocking mesh of proteoglycans, which provides compressive stiffness by way of the flexibility to absorb and extrude water. Numerous other noncollagenous proteins also contribute to the distinctive properties of cartilage (Table 1-1). However, this look is misleading because important topographical and regional differences exist within the molecular organization and composition of the articular cartilage, as described in Chapter 3. In mature articular cartilage, proteoglycans and different noncollagen proteins are turned over slowly, whereas the collagen network is secure until exposed to proteolytic cleavage. Proteins which may be related to chondrocyte cell membranes are also listed as a result of they allow specific interactions with extra-cellular matrix proteins. The particular structure-function relationships are mentioned in Chapter 3 and described in Table 3-1. The so-called tidemark defines the transition zone between the articular and calcified cartilage. This complicated biocomposite of bone and calcified cartilage supplies an optimal system for distributing masses that are transmitted from the weightbearing surfaces which are lined by the hyaline articular cartilage. Although the tidemark was originally believed to kind a barrier to fluid move, proof reveals that biologically lively molecules can transit this zone, offering a mechanism by which merchandise produced by chondrocytes or bone cells can influence the exercise of the opposite cell type. The subchondral bone undergoes steady structural reorganization all through postnatal life. These alterations are mediated by the coordinated exercise of bone-resorbing osteoclasts and bone-forming osteoblasts that rework and adapt the bone in response to native biomechanical and biological signals. These results are mediated via both cell-cell interactions with osteoclasts and osteoblasts but in addition by way of signaling via the release of soluble mediators. Note the clear demarcation of the articular cartilage from the calcified cartilage under the tidemark and the underlying subchondral bone. Alternatively, it has been proposed that changes in subchondral bone stiffness may be a result of cartilage deterioration. These structural alterations in the articular cartilage and periarticular bone can also result in modification of the contours of the adjacent articulating surfaces, further contributing to the adverse biomechanical surroundings. Both are important for the nutrition and lubrication of adjacent avascular structures, together with tendons and articular cartilage, and for limiting adhesion formation and maintaining motion. Characterization and measurement of synovial fluid constituents have proved useful for the identification of regionally generated regulatory elements, markers of cartilage turnover, and the metabolic status of the joint, in addition to for the assessment of the consequences of therapy on cartilage homeostasis. However, interpretation of such information requires an understanding of the generation and clearance of synovial fluid and its various components. Synovial fluid is a mixture of a protein-rich ultrafiltrate of plasma and hyaluronan synthesized by synoviocytes. Proteins are present in synovial fluid at concentrations inversely proportional to molecular size, with synovial fluid albumin concentrations being about 45% of those in plasma. Concentrations of electrolytes and small molecules are equal to these in plasma. In contrast to ultrafiltration, lymphatic clearance of solutes is unbiased of molecular dimension. In addition, constituents of synovial fluid, corresponding to regulatory peptides, could additionally be degraded locally by enzymes, and low-molecular-weight metabolites may diffuse along concentration gradients into plasma. Because the volume of synovial fluid is decided by the amount of hyaluronan, water retention seems to be the major perform of this massive molecule. Tissue fluid round fenestrated endothelium displays plasma ultrafiltrate most carefully, with a low content material of hyaluronate compared with synovial fluid. Alternatively, locally generated or launched peptides, such as endothelin and substance P, could attain a lot larger perivascular concentrations than those measured in synovial fluid. However, the turnover time for hyaluronan in the normal joint (13 hours) is an order of magnitude slower than that of small solutes and proteins. Association with hyaluronan may lead to trapping of solutes within synovial fluid. In regular joints, intra-articular pressures are barely subatmospheric at relaxation (0 to -5 mm Hg). Resting intra-articular pressures in rheumatoid joints are around 20 mm Hg, whereas during isometric exercise, they may increase to higher than one hundred mm Hg, nicely above capillary perfusion strain and, at instances, above arterial stress. Repeated mechanical stresses can interrupt synovial perfusion throughout joint movement, notably within the presence of a synovial effusion. A wide selection of regulatory components and merchandise of synoviocyte metabolism and cartilage breakdown may be generated regionally inside the joint, leading to marked differences between the composition of synovial fluid and plasma ultrafiltrate. Because little capacity exists for the selective concentration of solutes in synovial fluid, solutes which are current at larger concentrations than in plasma are probably synthesized regionally. It is necessary, nonetheless, to know the local clearance rate to decide whether or not the solutes current in synovial fluid at decrease concentrations than in plasma are generated domestically. Plasma proteins are much less successfully filtered in infected synovium, maybe because of elevated dimension of endothelial cell fenestrations or as a end result of interstitial hyaluronate-protein complexes are fragmented by enzymes associated with the inflammatory process. In inflammatory arthritis, fibrin deposits might retard move between the tissue and the liquid section. They speculated that the presence of those plasma proteins in the synovial fluid might be associated to alterations in the endothelial barrier associated with native irritation in the synovial tissue. They recognized 18 proteins that have been significantly differentially expressed between the osteoarthritic and management teams. Although the entire differentially expressed proteins have been current in the blood and will therefore enter the joint by way of alterations in vascular permeability associated with the disease state, these molecules had been additionally products of synovial cells and chondrocytes, suggesting that they could probably be domestically produced throughout the joint. They additionally identified members of the proinflammatory complement cascade in the synovial fluid. Dipalmitoyl phosphatidylcholine, which constitutes 45% of the lipid in regular synovial fluid, acts together with lubricin as a boundary lubricant. Vascularization of cartilage would be expected to alter its mechanical properties. Blood flow could be repeatedly occluded throughout weight bearing and exercise, with reactive oxygen species generated throughout reperfusion, resulting in repeated injury to cartilage matrix and chondrocytes. Chondrocytes synthesize specific inhibitors of angiogenesis that maintain articular cartilage as an avascular tissue. The synovial fluid and, indirectly, the synovial lining, by way of which synovial fluid is generated, are the major sources of nutrients for articular cartilage. Nutrients could enter cartilage from synovial fluid both by diffusion or by mass transport of fluid throughout compression-relaxation cycles. The idea has arisen from observations that joint immobilization or dislocation leads to degenerative adjustments. In distinction, train increases solute penetration into cartilage in experimental methods.
Grood E antifungal tube discount lotrisone 10 mg overnight delivery, Suntay W: A joint coordinate system for the medical description of three-dimensional motions: functions to the knee. Selvik G: A roentgen-stereophotogrammetric method for the study of the kinematics of the skeletal system, Lund, Sweden, 1974, University of Lund. Spoor C, Veldpaus F: Rigid physique motion calculated from spatial coordinates of markers. Myazaki T, Wada M, Kawahara H, et al: Dynamic load at baseline can predict radiographic disease development in medial compartment knee osteoarthritis. Tissue engineering has adopted the idea of biomimetics of in vivo tissue development. Developmental engineering is the time period used to describe novel methodology for the rational and correct design of sturdy, well-controlled manufacturing processes of "organic spare parts. Recent advances in regenerative medicine and tissue engineering relevant to rheumatology have entered scientific apply and embrace the biologic restore of joint floor defects and bone therapeutic. Destruction of joint tissues is finally the disabling outcome of most types of inflammatory or degenerative arthritides. The need for repair and regeneration of joints and joint-associated tissues is changing into extra related as the dramatic advances of focused therapies and improved disease management have allowed much more environment friendly management of irritation and joint destruction. In view of this example, different elements of joint biology deserve extra attention-notably, and most significantly, the mechanisms driving tissue response and restore. Introducing regenerative drugs offers a significant opportunity to restore joint homeostasis and thus possibly present a cure. Targeting restore has entered our self-discipline, and investigating the potential to activate and enhance joint tissue restore mechanisms has turn out to be a major aim. Nature demonstrates that this objective 90 is achievable, because profitable wound therapeutic and fracture repair are processes that occur routinely after birth. We also know, as demonstrated in fetal surgery, that scarless repair is partially dependent on age and context. For example, it seems that the method of rebuilding an grownup limb, such as seen in the axolotl, but additionally during fracture therapeutic in greater species, has many similarities with how the limb forms in the first place within the embryo, and significantly requires signaling mechanisms to specify the final sample. Thus each limb formation and limb regeneration are more probably to use the identical molecular pathways. These advances not solely embody our understanding of the mechanisms of body axis formation and organogenesis but in addition spectacular progress in stem cell biology, including the regulation of stemness, stem cell niches, lineage specification and cell differentiation, and the critical molecular pathways involved. The first strategy consists of enhancing intrinsic repair mechanisms with stimulation of cell proliferation, differentiation and tissue metabolic activity, and recruitment of endogenous progenitor populations into the damaged tissue. The severity and consequence of disease is decided by the steadiness between inflammation/destructive processes and anti inflammatory indicators with restore attempts. Although the evidence for the heritability of cartilage restore capacity in people continues to be circumstantial, findings of animal studies are extra convincing. Comparing the capacity of various inbred mouse strains to heal full-thickness cartilage defects, Eltawil et al. This finding helps the concept that the restore capability has a genetic element. Thus it was found that both the capability of healing joint floor defects and the capability to heal ear wounds have been extremely heritable and that they correlated with one another. Although Wnt signaling is important for the event and homeostasis of synovial joints,36-40 genetic research in humans20 and experimental data22,41,42 show that excessive/uncontrolled activation of Wnt/ catenin signaling results in reprogramming of articular chondrocytes toward catabolism or loss of their secure phenotype with subsequent loss of articular cartilage tissue structure and performance. In this chapter we select a quantity of examples of how these signaling pathways are involved in joint formation and their position in postnatal joint restore, with a specific concentrate on a few of these pathways which have led to advances in early clinical development in arthritic illnesses. It seems that a good control, both when it comes to timing and magnitude, is essential not solely to preserve homeostasis however even to induce tissue regeneration. In the medical context of joint disease and regeneration, the complexity of Wnt signaling and its potential downstream effects might provide the chance to goal catabolic effects whereas preserving the homeostatic ones. Better understanding of the downstream signaling mechanism and its regulation shall be important to goal solely the pathogenic effect of those pleiotropic signaling pathways in cartilage, bone, and the osteochondral junction. Growth Hormone/Insulin-like Growth Factor Axis Other targets in addition to skeletal developmental pathways are activated by signaling molecules that also play important roles in postnatal joint tissue homeostasis and turnover. These proteins/pathways can be thought to be potential postnatal "anabolic" agents that contribute to the restoration of joint homeostasis. Stem Cell Niches Stem cells persist in adult life to safeguard tissue maintenance and regeneration. They have the capability to selfrenew (that is, to produce more stem cells), thereby preserving a constant pool of stem cells, they usually have the capacity to differentiate to exchange the mature cells which are lost to physiologic turnover, harm, disease, or ageing. Self-renewal and differentiation are regulated by stem cell intrinsic components and signals from the surrounding microenvironment by which the stem cells reside, called the "stem cell area of interest. The joint setting is wealthy in progenitor/stem cells, but our understanding of their anatomic location in apposite niches and the molecular regulation of their capabilities stays restricted. It is probably going that, rather than having a common ancestor, pericytes have distinct ontogeny and biologic properties that are related to their tissues of residence. They could partly derive from the embryonic joint interzone, as lineage tracing research suggest. The restoration of a useful area of interest will safeguard sturdy restore by making certain lifelong substitute of mature cells. B, particulars of the dashed box in A, showing cell populations in the synovium of uninjured joints. C, schematic drawing of a synovial joint 12 days after articular cartilage damage in mice (arrowhead). Proliferating cells have been detected in each the synovial lining and the subsynovial tissue and have been either double optimistic for idu and chlorodeoxyuridine (Cidu; orange) or single positive for Cidu (red). Targeting Homeostasis of the Joint In the resting condition, articular cartilage has an especially low fee of turnover. After acute traumatic harm, nonetheless, chondrocytes deploy sturdy adaptive responses that in the end end in a coordinated sequence of activation and chemotaxis of progenitors within the cartilage itself and in other joint tissues, together with cell proliferation and matrix turnover. In a selection of circumstances, such adaptive responses are enough to repair harm and re-establish homeostasis. More correct molecular analyses have recognized several different components that are amenable for targeting. In the entire joint, inflammation is an integral part of a natural response to damage, offering molecular alerts and cascades which might be prone to have distinct context and tissue-specific useful or detrimental effects. Studies geared toward teasing apart the "good" from the "dangerous" pathways will assist modulate restore processes and restore/maintain joint homeostasis. Scarification of the articular cartilage in vitro or in vivo induces a strong early molecular response dominated by the activation of signaling pathways recognized to play essential roles in embryonic skeletogenesis. It is necessary to say right here, nonetheless, that though proof of concept for efficacy with each of these pathways has been provided ultimately in several fashions, the usually disparate functions that these pleiotropic signaling molecules have in every completely different cell sort stay a challenge. Tissue-targeted treatments might be of significance, together with using novel good supply techniques to confine the signaling area of such highly effective morphogens and avoid off-target effects. Yet the understanding of the pathophysiologic mechanisms driving stem cell commitment and differentiation is paving the greatest way to promising therapeutic interventions that exploit homeostatic mechanisms. In truth, recent knowledge show that kartogenin might help harmonious skeletal progress, joint morphogenesis, and the resorption of the interdigital mesenchyme, that are otherwise stunted in ex vivo cultures of embryonic mouse limbs. After the joint floor defect is filled with mesenchymal cells, the restore tissue needs patterning to acquire the final architectural construction, with a properly layered cartilage and osteochondral junction. Interestingly, both morphologically and molecularly, the repair tissue in an osteochondral defect resembles the epiphysis of a developing skeletal factor, with flat cells on the surface, then chondrocytes in numerous levels of maturation, and hypertrophic chondrocytes on the boundary with the bone front. Failure of this patterning process leads to failure of restore both in animal models87,88 and also in people, where excessive development of the bone front can result in intra-articular osteophytes after surgical procedures such as bone marrow stimulation by microfracture. Unfortunately, the doses required to achieve this spectacular effect in mice have been very high and induced osteopetrosis. A restriction of the signaling domains to the tissue of curiosity is due to this fact required earlier than this method can be used in the clinic. The mechanisms via which the cellular therapies and combination merchandise contribute to tissue restore are multiple and involve direct engraftment, proliferation, and differentiation to tissue-specific cell sorts but in addition include paracrine actions such because the secretion of progress and differentiation components that improve the native tissue response. Joint Surface Defects A variety of articular cartilage restore strategies have been developed, sometimes for the remedy of (sub)acute focal joint surface defects which may be typically related to extreme joint loading, both on account of high-impact trauma or cumulative low-impact repetitive overload. Joint floor lesions can prolong to the subchondral bone (osteochondral defects) or be restricted to the cartilage (chondral defects). The greatest established cell-based expertise for the therapy of those lesions is autologous chondrocyte transplantation and its several variations. Autologous Chondrocyte Transplantation Regeneration or repair of symptomatic articular cartilage defects has been on the forefront of regenerative medication ever since 1994 when Brittberg et al.
Consequently antifungal cream for jock itch in india lotrisone 10 mg buy low cost, neutrophil 2 integrins fail to type, and bloodstream neutrophils are unable to adhere firmly to vascular endothelium and transmigrate to websites of infection. The clinical picture is similar to that of the neutropenias, with recurrent life-threatening infections. Peripheral neutrophil counts are sometimes elevated, nonetheless, reflecting the intravascular accumulation of cells within the face of their lack of ability to exit the vessels. In addition, rare congenital problems of neutrophils have been identified (Table 11-2). In common, patients with congenital impaired neutrophil operate are susceptible to infection by bacteria (predominantly Staphylococcus aureus, Pseudomonas species, Burkholderia) and fungi. The major websites of an infection embrace pores and skin, mucous membranes, and lungs, but any website may be affected, and spreading abscesses are common. Most of these ailments are potentially life threatening within the absence of accessible efficient therapy. Monogenic autosomal dominant, autosomal recessive, sporadic, and polygenic subtypes have been recognized. Because of the lack of acute irritation, infections are inclined to spread extensively before being noted, and the mortality fee is high. Therapy Granule Defects Ch�diak-Higashi syndrome is an autosomal recessive disorder by which granule subtypes-in neutrophils, lymphocytes, melanocytes, Schwann cells, and others-undergo disordered fusion, resulting in big, dysfunctional granules. Patients with this syndrome have congenital neutropenia with structurally abnormal neutrophil major granules and abnormalities of B cells, cytotoxic T cells, and melanocytes. In addition to immunodeficiency, medical findings embody brief stature and partial albinism. As a results of the inability to kill organisms, accumulation of neutrophils at a website of an infection typically ends in granuloma formation, quite than clearance of the target. The presence of even partially responsive neutrophils leads to a lower frequency of sepsis in these patients relative to patients with absolute neutropenia. Intra-articular urate crystals nonspecifically bind immunoglobulin and activate complement by the traditional and alternative pathways. Neutrophils in the gouty joint may harm joint constructions through discharge of contents directly into the joint fluid during crystal phagocytosis or instantly towards cartilage during attempted phagocytosis of urate crystals embedded in or adherent to cartilage. Interaction of phagocytosed urate crystals with lysosomal membranes additionally ends in the dissolution of the latter, spilling lysosomal proteases into the cytoplasm and, eventually, into the extra-cellular area. Several mechanisms may allow the discharge of neutrophil proteases and oxygen radicals into the extra-cellular milieu. First, necrosis or destruction of neutrophils, or each, could liberate cellular contents indiscriminately. Second, studies have revealed that degranulation and O2- technology may begin earlier than complete closure of the phagocytic vacuole, releasing products either into the external setting (regurgitation throughout feeding) or against a target floor. Although serum and joint fluid contain anti-proteases and antioxidants, the "protected house" between a neutrophil and a floor. In the synovium, lymphocytes, fibroblasts, and macrophages predominate, however the joint house contains mainly neutrophils. Neutrophil defensins improve phagocytosis by macrophages and stimulate the activation and degranulation of mast cells, an interesting observation in light of a report that mice deficient in mast cells are resistant to the development of erosive arthritis. Systemic Lupus Erythematosus Until recently, the role of the neutrophil in lupus was thought-about to be restricted to its operate as an inflammatory effector. The early observation that infusions of allospecies serum produced acute irritation in skin and joints (serum sickness), together with the appreciation that subcutaneous re-challenge with beforehand administered antigen results in intense native inflammation (the Arthus reaction), led to the development of a mannequin during which immune advanced deposition in blood vessels ends in complement activation and an influx of neutrophils. Because immune complicated formation is a hallmark of many small vessel vasculitides. In several of those situations, neutrophil disruption and fragmentation-clasis-is a distinguished pathologic finding, resulting in their designation beneath the rubric leukocytoclastic vasculitis. It has been instructed that sufferers with lupus expertise transient accumulations of neutrophils (leukoaggregation) in small vessels of the lungs and different tissues as a result of complement activation inside these vessels or in the soluble part. The Shwartzman phenomenon, during which reinjection of mobile material leads to vascular inflammation by way of a cytokine-dependent, immune complex� independent mechanism, is a mannequin for this avenue to vasculitis. It is likely that many rheumatic ailments employ each immune complex�dependent and immune complex�independent mechanisms within the pathogenesis of neutrophil ingress into vascular buildings. Histopathologic options are characterised by dense neutrophilic infiltrate in the superficial dermis and edema of the dermal papillae and papillary dermis. Leukocytoclasia might recommend leukocytoclastic vasculitis, although vascular injury is absent. Treatment with systemic corticosteroids normally induces a dramatic decision of the lesions and the systemic symptoms. Pyoderma gangrenosum is characterised by painful ulcerating cutaneous lesions over the lower extremities, usually in patients with an underlying inflammatory illness. Other rare neutrophilic dermatoses embrace rheumatoid neutrophilic dermatitis, described as symmetric erythematous nodules on extensor surfaces of joints; bowel-associated dermatosisarthritis syndrome occurring after bowel bypass surgical procedure for weight problems; and neutrophilic eccrine hidradenitis, which is typically linked to acute myelogenous leukemia. In familial Mediterranean fever (discussed in detail in Chapter 97), sufferers expertise episodic inflammatory exacerbations characterised by giant influxes of neutrophils. A defect within the regulatory protein pyrin appears to permit the inappropriate growth of inflammation, leading to its categorization as an autoinflammatory illness. Pyrin is expressed primarily in myeloid cells, including neutrophils and eosinophils. Glucocorticoids Glucocorticoids exert potent effects on neutrophils, including inhibition of neutrophil phagocytic activity and adhesive perform. The capability of steroids to enhance peripheral blood neutrophil populations acutely-an impact generally identified as demargination-is attributable to both a launch of neutrophils from the bone marrow and the discharge (demargination) of neutrophils adherent to vessel partitions. Effects of glucocorticoids on different cells can also cut back neutrophil responses not directly through the suppression of cytokines at inflammatory websites. Disease-Modifying Anti-rheumatic Drugs Several disease-modifying anti-rheumatic medication have wellestablished effects on neutrophils. Because pyrin deficiencies are implicated in familial Mediterranean fever, this statement suggests a previously unappreciated mechanism of action of colchicine in neutrophilic illnesses. Murdoch C, Finn A: Chemokine receptors and their position in irritation and infectious illnesses. Protein kinase C promotes cytoskeletal and membrane affiliation of cytosolic oxidase elements. Gautam N, Herwald H, Hedqvist P, et al: Signaling by way of beta(2) integrins triggers neutrophil-dependent alteration in endothelial barrier function. When improperly regulated, nonetheless, these similar mechanisms turn into the idea of inflammatory and autoinflammatory illness and potentially result in tissue destruction. In several rheumatic illnesses, the neutrophil subsequently serves not merely as an effector cell however as a direct participant in disease pathogenesis. Chen F, Wu W, Millman A, et al: Neutrophils prime a long-lived effector macrophage phenotype that mediates accelerated helminth expulsion. Borregaard N, Lollike K, Kjeldsen L, et al: Human neutrophil granules and secretory vesicles. Chironi G, Simon A, Hugel B, et al: Circulating leukocyte-derived microparticles predict subclinical atherosclerosis burden in asymptomatic subjects. Arita M, Bianchini F, Aliberti J, et al: Stereochemical task, antiinflammatory properties, and receptor for the omega-3 lipid mediator resolvin E1. Weissmann G, Spilberg I, Krakauer K: Arthritis induced in rabbits by lysates of granulocyte lysosomes. Skokowa J, Germeshausen M, Zeidler C, et al: Severe congenital neutropenia: inheritance and pathophysiology. Bohn G, Allroth A, Brandes G, et al: A novel human main immunodeficiency syndrome attributable to deficiency of the endosomal adaptor protein p14. Tortorella C, et al: Spontaneous and Fas-induced apoptotic cell death in aged neutrophils. Dewald B, Bretz U, Baggiolini M: Release of gelatinase from a novel secretory compartment of human neutrophils. Nomura S, Ozaki Y, Ikeda Y: Function and function of microparticles in varied medical settings. Germeshausen M, Zeidler C, Stuhrmann N, et al: Digenic mutations in severe congenital neutropenia.
Lotrisone 10 mg generic with visa. Antibiotics Made Easy: Antifungals.
References
Tabouret E, Chinot O, Metellus P, et al. Recent trends in epidemiology of brain metastases: an overview. Anticancer Res 2012; 32(11):4655-4662.
Haddad, A. (1991). The nurse-physician relationship and ethical decision-making. AORN, 53(1), 151-156.
Li L, Jiang Q, Ding G, et al. Effects of administration route on migration and distribution of neural progenitor cells transplanted into rats with focal cerebral ischemia, an MRI study. J Cereb Blood Flow Metab 2010;30:653-62.
Raza SJ, Guru K: Conventional laparoscopic surgery: more pain, no gain! Editorial comment, BJU Int 2015.
Tanaka M, Itoh K, Matsushita K, et al: Two male siblings with hereditary renal hypouricemia and exercise-induced ARF, Am J Kidney Dis 42:1422n1493, 2003.
James AE Jr, Montali RJ, Chaffee V, et al: Barium or Gastrografin: Which contrast media for diagnosis of esophageal tears? Gastroenterology 68:1103, 1975.
Hendlin, K., Lee, C., Anderson, J.K., Monga, M. Radial dilation force of tipless and helical stone baskets. J Endourol 2004;18:946-947.
Peterson AL, Quartermain MD, Ades A, et al. Impact of mode of delivery on markers of perinatal hemodynamics in infants with hypoplastic left heart syndrome. J Pediatr. 2011;159:64-69.
