Corrigendum to "Angle-dependent spectral reflectance material dataset based on 945 nm time-of-flight camera measurements" Data in Brief 48 (2023) 109031.

[This corrects the article DOI: 10.1016/j.dib.

Angle-dependent spectral reflectance material dataset based on 945 nm time-of-flight camera measurements.

The main objective of this article is to provide angle-dependent spectral reflectance measurements of various materials in the near infrared spectrum. In contrast to already existing reflectance libraries, e.g.

Towards a novel continuous HME-Tableting line: Process development and control concept.

The objective of this study was to develop a novel closed-loop controlled continuous tablet manufacturing line, which first uses hot melt extrusion (HME) to produce pellets based on API and a polymer matrix. Such systems can be used to make complex pharmaceutical formulations, e.g.

Ensuring tablet quality via model-based control of a continuous direct compaction process.

Switching from batch to continuous pharmaceutical production offers several advantages, such as an increased productivity, a steady product quality, and decreased costs. This paper presents a control strategy for direct compaction on a continuous tablet production line consisting of two feeders, one blender, and a tablet press (TP). A data-driven, linear modeling approach is applied in order to develop a Smith predictor for active pharmaceutical ingredient concentration control and a model predictive controller responsible for the TP hopper level.

Chronic endothelin-A receptor antagonism is as protective as angiotensin converting enzyme inhibition against cardiac dysfunction in diabetic rats.

Background And Purpose: Diabetes mellitus is associated with a specific cardiomyopathy. We compared the cardioprotective effects of an endothelin-A receptor blocker (ET(A)-RB) with those of an angiotensin-converting enzyme inhibitor (ACE-I) in rats with streptozotocin (STZ)-induced diabetes.

Experimental Approach: Diabetic rats were left untreated or received either the ET(A)-RB atrasentan or the ACE-I ramipril (each 3 mg kg(-1) per day) orally for 8 weeks.

Cardioprotective effects of atrasentan, an endothelin-A receptor antagonist, but not of nitric oxide in diabetic mice with myocyte-specific overexpression of endothelial nitric oxide synthase.

1. We investigated the roles of nitric oxide (NO) and endothelin-1 (ET-1) in organ dysfunction in diabetic mice with normal genotype (wild-type, WT) or myocyte-specific overexpression of endothelial NO synthase (eNOS) (transgenic, TG) after chronic oral treatment with the endothelin-A (ETA) receptor antagonist atrasentan. 2.

Effects of chronic endothelin ET(A) receptor blockade on blood pressure and vascular formation of cyclic guanosine-3',5'-monophosphate in spontaneously hypertensive rats.

Endothelin (ET) mediates vasoconstriction in intact arterial blood vessels with functional endothelium via stimulation of ET(A) receptors, while ET(B) receptor stimulation leads to vasodilation via nitric oxide (NO) release and formation of cyclic guanosine-3',5'-monophosphate (cGMP). In spontaneously hypertensive rats (SHR) the cGMP-forming NO-receptor guanylyl cyclase (sGC) is downregulated. It is unclear whether ET contributes to the hypertensive phenotype of SHR, and whether this involves the disturbed cGMP signaling.

The role of endothelin receptor antagonists in cardiovascular pharmacotherapy.

Endothelin (ET) is a hormone produced predominantly by endothelial cells which has been recognised to play a significant role in the development of several cardiovascular disease states. In order to combat the deleterious effects of ET, several ET-receptor antagonists (ETRA) are currently in clinical development. The agents developed thus far inhibit the actions of ET through either selective inhibition of the ET(A) receptors or non-selective inhibition of both ET(A) and ET(B) receptors.

Endothelin receptor antagonists: clinical realities and future directions.

Endothelin (ET) is among the strongest endogenous vasoconstrictors known and a potent mitogen. A rich body of experimental evidence suggests that ET contributes to vascular remodeling and end-organ damage in several cardiovascular conditions. Therefore, blockade of ET receptors has been suggested as an attractive target in a number of acute and chronic cardiovascular indications, including pulmonary arterial hypertension (PAH), systemic hypertension, and heart failure.

Nonviral monocyte chemoattractant protein-1 gene transfer improves arteriogenesis after femoral artery occlusion.

Local infusion of recombinant monocyte chemoattractant protein-1 (MCP-1) has been shown to enhance collateral artery formation in rabbit and pig hindlimb models. Owing to clinical disadvantages of protein infusion, a nonviral, liposome-based MCP-1 gene transfer was developed. Collateralization in a porcine hindlimb model served to provide a proof-of-principle for the functional benefit of MCP-1 overexpression.

[Endothelin receptor block in acute pancreatitis--improvement of microcirculation and decrease of capillary permeability also distant from the pancreas].

We have previously demonstrated that therapy with a new specific endothelin-1 receptor antagonist (ET-RA) significantly reduced mortality in acute necrotizing pancreatitis (ANP) in the rat. Improved survival was not associated with decreased intrapancreatic trypsinogen activation or parenchymal necrosis but with reduced fluid sequestation into the third space suggesting that ET-RA counteracts systemic rather than local sequelae of severe pancreatitis. The present study further tests this hypothesis by evaluating the effect of the specific ET-1 antagonist LU-135252 on capillary blood flow, capillary density, and capillary permeability not only in the pancreas but also in the colon, and monitoring fluid losses and renal and respiratory function.

Influence of acute selective endothelin-receptor-A blockade on renal hemodynamics in a rat model of chronic allograft rejection.

We have recently demonstrated up-regulation of renal endothelin (ET) synthesis in a rat model of chronic renal allograft rejection. Treatment with a selective ET-A receptor antagonist improved survival and reduced functional and morphological kidney damage. However, the underlying mechanisms have not yet been elucidated, as ET exhibits both hemodynamic and inflammatory properties.

Effects of the endothelin a receptor antagonist darusentan on blood pressure and vascular contractility in type 2 diabetic Goto-Kakizaki rats.

The present study evaluated the effects of long-term treatment with the endothelin A (ET(A)) receptor antagonist darusentan (LU135252) on blood pressure (BP) and vascular target-organ damage in spontaneously type 2 diabetic Goto-Kakizaki (GK) rats. BP was monitored by radiotelemetry in untreated and darusentan-treated GK rats from 10-24 weeks of age. Relaxation of mesenteric artery segments by acetylcholine (ACh) and sodium nitroprusside (SNP) was measured to assess endothelium-dependent and -independent vasorelaxation.

Selectivity of different calcium antagonists on T- and L-type calcium currents in guinea-pig ventricular myocytes.

Both L- and T-type calcium channels are present in the heart. In cardiac myocytes L-type calcium channels are blocked by the classical calcium channel blockers, while T-type calcium channels are thought to be insensitive to these drugs and to be selectively blocked by mibefradil. We aimed to compare the T/L calcium channel blocking selectivity of several calcium channel blockers by evaluating their effects on both components evoked in the same cell from a holding potential corresponding to the normal physiological value (-90mV).

Trauma induced by nontraumatic coronary devices and its impact on vascular reactivity and morphology.

This study evaluated the impact of low-pressure balloon devices on coronary morphology and function. An active coronary perfusion catheter (2.5-mm balloon diameter, inflation with 1 bar for 30 min) was placed in the left anterior descending coronary artery of 12 German landrace pigs under general anesthesia.

Endothelin A-receptor antagonist administration immediately after experimental myocardial infarction with reperfusion does not affect scar healing in dogs.

Objective: Endothelin (ET) receptor antagonists have been reported to reduce both infarct size and no-reflow phenomenon; however, in rat models their effect on the healing process after myocardial infarction (MI) is controversial. The study aimed to evaluate the effect of early administration of the ET(A) receptor antagonist darusentan on scar healing in an ischemia-reperfusion model in dogs.

Methods: Thirty male mongrel dogs surviving 180 min left anterior descending coronary artery balloon occlusion were randomised to: darusentan i.

Endothelin receptor blockade and in-stent restenosis.

The aim of the present study was to test whether oral dosing of an endothelin (ET) receptor antagonist was able to reduce restenosis in the model of stent-induced restenosis. After pigs underwent coronary artery catheterization they were randomly allocated either to controls or to treatment with the ET receptor antagonist BSF 208075. Thirty-seven pigs underwent percutaneous transluminal coronary angioplasty plus stent implantation; seven animals died of ventricular fibrillation due to procedure-related myocardial ischaemia.

Therapeutic administration of an endothelin-A receptor antagonist after acute ischemic renal failure dose-dependently improves recovery of renal function.

Endothelin (ET) is known to reduce glomerular filtration rate and renal blood flow and is a possible mediator of acute renal failure (ARF). We recently demonstrated that the administration of a very high dose of the ET(A)-receptor antagonist LU 135252 (LU) accelerates recovery from postischemic acute renal failure by an improvement of renal perfusion in a rat model. The aim of this study was to investigate whether this effect of LU is dose dependent.

Endothelin mediates local and systemic disease sequelae in severe experimental pancreatitis.

Endothelin-1 has been shown to reduce pancreatic blood flow and cause focal acinar cell necrosis similar to those seen in acute pancreatitis (AP), whereas therapy with endothelin receptor antagonists enhanced pancreatic capillary blood flow (PCBF) and decreased mortality rates. The current study evaluated the role of endothelin in the development of severe AP. Trypsinogen activation peptides, acinar cell necrosis, and PCBF were used as local indicators of disease severity, fluid sequestration, cardiorespiratory and renal parameters, and colonic capillary blood flow as systemic disease indicators.

Improvement of renal dysfunction in rats with chronic heart failure after myocardial infarction by treatment with the endothelin A receptor antagonist, LU 135252.

Objective: To investigate the role of an activated endothelin system in the renal dysfunction observed in chronic heart failure after myocardial infarction.

Methods: In rats with heart failure after myocardial infarction and in sham-operated animals (Sham), we investigated the effect on renal function of long-term oral treatment with the selective endothelin A (ETA) receptor antagonist, LU 135252 (30 mg/kg per day; groups MI/LU and Sham/LU) or placebo (groups MI/P, Sham/P). Only animals with extensive myocardial infarction (at least 46% of the left ventricle) were included in the study.

Treatment with a combined endothelin A/B-receptor antagonist does not prevent chronic renal allograft rejection in rats.

A markedly increased expression of endothelin (ET)-1 has been observed in renal allografts with chronic rejection, one of the most common causes of kidney graft loss. In this study we investigated the effect of treatment with a combined ET-A/B-receptor antagonist on the course of chronic renal allograft rejection. Experiments were performed in the Fisher-to-Lewis rat model of chronic rejection.

Endothelin receptor blockade in severe acute pancreatitis leads to systemic enhancement of microcirculation, stabilization of capillary permeability, and improved survival rates.

Background: We previously demonstrated that therapy with a new endothelin A receptor antagonist (ET-RA) significantly reduced mortality rates in severe acute pancreatitis (AP) in the rat without attenuating local signs of disease severity (intrapancreatic protease activation, acinar cell necrosis). This raised the question as to why ET-RA was so effective. The purpose of this study was to assess the effect of ET-RA on microcirculation (particularly capillary permeability) within and outside of the pancreas on intravascular fluid loss and extravascular fluid sequestration and on distant organ function.

Improved recovery following posttransplant acute renal failure in rat renal isografts with an oral endothelin-A receptor antagonist.

Background: Delayed renal function after transplantation is a strong predictor of long-term graft survival. As an increased expression of endothelin (ET) has been demonstrated during ischemia/reperfusion injury, we hypothesized that ET-A receptor blockade could improve the recovery of acute renal failure in a rat model of isogeneic kidney transplantation.

Methods: Kidneys of Fisher (F344, RT1(1v1)) rat donors flushed with cooled University of Wisconsin solution were transplanted into bilaterally nephrectomized Fisher rats.

Synergistic effects of AT(1) and ET(A) receptor blockade in a transgenic, angiotensin II-dependent, rat model.

Angiotensin II and endothelin may participate in increasing blood pressure and inducing end-organ damage, but the evidence is conflicting. We tested the hypothesis that endothelin(A) receptor blockade would ameliorate blood pressure and end-organ damage in a rat model of human renin-dependent hypertension. We studied rats that were transgenic for both the human renin and angiotensinogen genes.