Of course, all routes and controllers should return some kind of response to be sent back to the user's browser. Lumen provides several different ways to return responses. The most basic response is simply returning a string from a route or controller:
However, for most routes and controller actions, you will be returning a full Illuminate\Http\Response instance. Returning a full Response instance allows you to customize the response's HTTP status code and headers. A Response instance inherits from the Symfony\Component\HttpFoundation\Response class, providing a variety of methods for building HTTP responses:
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Keep in mind that most response methods are chainable, allowing for the fluent building of responses. For example, you may use the header method to add a series of headers to the response before sending it back to the user:
The response helper may be used to conveniently generate other types of response instances. When the response helper is called without arguments, an implementation of the Illuminate\Contracts\Routing\ResponseFactory contract is returned. This contract provides several helpful methods for generating responses.
The download method may be used to generate a response that forces the user's browser to download the file at the given path. The download method accepts a file name as the second argument to the method, which will determine the file name that is seen by the user downloading the file. Finally, you may pass an array of HTTP headers as the third argument to the method:
Redirect responses are instances of the Illuminate\Http\RedirectResponse class, and contain the proper headers needed to redirect the user to another URL. There are several ways to generate a RedirectResponse instance. The simplest method is to use the global redirect helper method:
When you call the redirect helper with no parameters, an instance of Laravel\Lumen\Http\Redirector is returned, allowing you to call any method on the Redirector instance. For example, to generate a RedirectResponse to a named route, you may use the route method:
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The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.
Introduction: To compare the utility of the distensibility index (DI) on functional lumen imaging probe (FLIP) topography to other esophagogastric junction (EGJ) metrics in assessing treatment response in achalasia in the context of esophageal anatomy.
Methods: We prospectively evaluated 79 patients (at ages 17-81 years; 47% female patients) with achalasia during follow-up after pneumatic dilation, Heller myotomy, or per-oral endoscopic myotomy with timed barium esophagram, high-resolution impedance manometry, and FLIP. Anatomic deformities were identified based on consensus expert opinion. Patients were classified based on anatomy and EGJ opening to determine the association with radiographic outcome and Eckardt score (ES).
Discussion: The FLIP DI is most useful metric for assessing the effect of achalasia treatment on EGJ opening. However, abnormal anatomy is an important mediator of outcome and treatment success will be modulated by anatomic defects that impede bolus emptying.
Neutrophil infiltration into tissues is essential for host defense and pathogen clearance. Although many of the signaling pathways involved in the transendothelial migration of neutrophils are known, the role of the endothelium in regulating neutrophil behavior in response to infection within interstitial tissues remains unclear. Here we developed a microscale 3-dimensional (3D) model that incorporates an endothelial lumen, a 3D extracellular matrix, and an intact bacterial source to model the host microenvironment. Using this system, we show that an endothelial lumen significantly increased neutrophil migration toward a source of Pseudomonas aeruginosa Surprisingly, we found neutrophils, which were thought to be short-lived cells in vitro, migrate for up to 24 hours in 3D in the presence of an endothelial lumen and bacteria. In addition, we found that endothelial cells secrete inflammatory mediators induced by the presence of P aeruginosa, including granulocyte-macrophage colony-stimulating factor (GM-CSF), a known promoter of neutrophil survival, and interleukin (IL)-6, a proinflammatory cytokine. We found that pretreatment of neutrophils with a blocking antibody against the IL-6 receptor significantly reduced neutrophil migration to P aeruginosa but did not alter neutrophil lifetime, indicating that secreted IL-6 is an important signal between endothelial cells and neutrophils that mediates migration. Taken together, these findings demonstrate an important role for endothelial paracrine signaling in neutrophil migration and survival.
Background: Based on stoichiometric assumptions, and real-time assessment of expired carbon dioxide (%CO2) and flow rate, the Lumen device provides potential for consumers/athletes to monitor metabolic responses to dietary programs outside of laboratory conditions. However, there is a paucity of research exploring device efficacy. This study aimed to evaluate Lumen device response to: i) a high-carbohydrate meal under laboratory conditions, and ii) a short-term low- or high-carbohydrate diet in healthy volunteers.
Conclusion: Our findings demonstrated that a portable, home-use metabolic device (Lumen) detected significantly increased expired %CO2 in response to a high-carbohydrate meal, and may be useful in tracking mean weekly changes to acute dietary carbohydrate modifications. Additional research is warranted to further determine the practical and clinical efficacy of the Lumen device in applied compared to laboratory settings.
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Congenital obstructive nephropathy (CON) is the most prevalent cause of pediatric chronic kidney disease and end-stage renal disease. The ureteropelvic junction (UPJ) region, where the renal pelvis transitions to the ureter, is the most commonly obstructed site in CON. The underlying causes of congenital UPJ obstructions remain poorly understood, especially when they occur in utero, in part due to the lack of genetic animal models. We previously showed that conditional inactivation of Sec10, a central subunit of the exocyst complex, in the epithelial cells of the ureter and renal collecting system resulted in late gestational bilateral UPJ obstructions with neonatal anuria and death. In this study, we show that without Sec10, the urothelial progenitor cells that line the ureter fail to differentiate into superficial cells, which are responsible for producing uroplakin plaques on the luminal surface. These Sec10-knockout urothelial cells undergo cell death by E17.5 and the urothelial barrier becomes leaky to luminal fluid. Also at E17.5, we measured increased expression of TGF1 and genes associated with myofibroblast activation, with evidence of stromal remodeling. Our findings support the model that a defective urothelial barrier allows urine to induce a fibrotic wound healing mechanism, which may contribute to human prenatal UPJ obstructions.
Ureter development in mice begins at embryonic day 10.5 (E10.5) when the ureteric bud grows from the nephric duct in response to signals from the metanephric mesenchyme. As the tip of the ureteric bud grows and branches into the metanephric mesenchyme to become the kidney, the stalk elongates to form the ureter. The base of the ureteric bud migrates down the nephric duct and eventually connects directly with the bladder11. Although the ureteric bud starts as a single monolayer of epithelial cells, it induces development of an outer smooth muscle layer and then differentiates into a multilayered transitional epithelium called the urothelium. Lining the renal pelvis, ureter, bladder and urethra, the urothelium is both flexible and fluid impermeable to allow stretching while preventing urine from escaping the lumen of the urinary tract. In order to do this, the lumen-facing superficial cells of the urothelium produce very high levels of transmembrane proteins called uroplakins, which form hexagonal plaques on the luminal surface12,13,14,15. These uroplakin plaques cover a majority of the apical plasma membrane and are connected by flexible hinge regions. The four members of the uroplakin family (Upk1a, Upk1b, Upk2 and Upk3) are transmembrane proteins that assemble into heterodimers in the ER (Upk1a-Upk2 and Upk1b-Upk3) before being trafficked through the Golgi and to the apical surface in discoid/fusiform vesicles13. A pool of these uroplakin-containing vesicles are maintained under the apical surface of the mature superficial cells and the dynamic exocytosis and endocytosis allows the urothelial surface area to expand and contract in response to mechanical stretch16,17. High expression of the uroplakin family members and formation of these plaques is critical for the development and maintenance of the urothelial barrier.
These mice had bilateral UPJ obstructions late in gestation, between E17.5 and E18.5, due to a cellular overgrowth that filled the ureter lumen18. This overgrowth was composed of mesenchymal shaped cells positive for smooth muscle actin (SMA), with an almost complete disappearance of E-cadherin-positive urothelial cells. Analysis of the Sec10FL/FL;Ksp-Cre ureters at E17.5 identified an absence of uroplakin-3 (Upk3) on the superficial surface of the urothelium. In addition, a higher proliferation rate of SMA-positive cells was measured at the UPJ region in these ureters at E17.5, prior to the obstruction of the ureter lumen. 152ee80cbc
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