Spectrophotometric estimation of tamsulosin hydrochloride by acid-dye method

Shrivastava, Aviral; Saxena, Prachi; Gupta, Vipul

doi:10.4103/2229-4708.81089

Cited by 11 publications

(5 citation statements)

References 15 publications

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“…PERG signals were recorded simultaneously from both eyes from subdermal electrodes in the snout in response to horizontal bars that maximized PERG amplitude and minimized the noise (spatial frequency 0.05 cycles/deg, temporal frequency 1 Hz, contrast 100%, robust averaging of 2232 sweeps). The PERG signal-to-noise ratio was of the order of 10, and the test-retest variability was of the order of 30% [52]. Balanced salt solution (BSS) drops were applied to maintain cornea hydration.…”

Section: Methodsmentioning

confidence: 99%

Inflammasome-Dependent Dysfunction and Death of Retinal Ganglion Cells after Repetitive Intraocular Pressure Spikes

Spurlock,

An,

Reshetnikova

et al. 2023

Preprint

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Dysfunction and selective loss of retinal ganglion cells (RGCs) is a known cause of vision loss in glaucoma and other neuropathies where ocular hypertension (OHT) is the major risk factor. We investigated the impact of transient non-ischemic OHT spikes (spOHT) on RGC function and viability in vivo to identify cellular pathways linking low-grade repetitive mechanical stress to RGC pathology. We found that repetitive spOHT had an unexpectedly high impact on intraocular homeostasis and RGC viability, while exposure to steady OHT (stOHT) of similar intensity and duration failed to induce pathology. The repetitive spOHT induced a rapid activation of the inflammasome, marked by the upregulation of NLRP1, NLRP3, AIM2, caspases -1, -3/7, -8, gasdermin D (GsdmD) and the release of interleukin-1β (IL-1β) and other cytokines into the vitreous. Similar effects were also detected after 5 weeks of exposure to chronic OHT in an induced glaucoma model. The onset of these immune responses in both spOHT and glaucoma models preceded a 50% deficit in pattern electroretinograms (PERG) amplitude, and significant loss of RGCs at 7 days post-injury. Inactivation of inflammasome complexes in NLRP1-/- , Casp1-/- and GsdmD-/- knockout animals, significantly suppressed the spOHT induced inflammatory response and protected RGCs. Our results demonstrate that mechanical stress produced by acute repetitive spOHT or chronic OHT is mechanistically linked to inflammasome activation, which leads to RGC dysfunction and death.

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Section: Methodsmentioning

confidence: 99%

Inflammasome-Dependent Dysfunction and Death of Retinal Ganglion Cells after Repetitive Intraocular Pressure Spikes

Spurlock,

An,

Reshetnikova

et al. 2023

Preprint

View full text Add to dashboard Cite

show abstract

“…The values from the wells containing blank samples were subtracted from the background. To validate the significance of measurements at the lowest reading, the limit of detection (LOD) and limit of quantification (LOQ) ratios were calculated from empirical data obtained in the "zero" wells of each plate, as described [49]. A minimum of three (N = 3) biological repeats were used for each data point.…”

Section: Intravitreal Cytokine Activity Assaymentioning

confidence: 99%

The Inflammasome-Dependent Dysfunction and Death of Retinal Ganglion Cells after Repetitive Intraocular Pressure Spikes

Spurlock,

An,

Reshetnikova

et al. 2023

Cells

View full text Add to dashboard Cite

The dysfunction and selective loss of retinal ganglion cells (RGCs) is a known cause of vision loss in glaucoma and other neuropathies, where ocular hypertension (OHT) is the major risk factor. We investigated the impact of transient non-ischemic OHT spikes (spOHT) on RGC function and viability in vivo to identify cellular pathways linking low-grade repetitive mechanical stress to RGC pathology. We found that repetitive spOHT had an unexpectedly high impact on intraocular homeostasis and RGC viability, while exposure to steady OHT (stOHT) of a similar intensity and duration failed to induce pathology. The repetitive spOHT induced the rapid activation of the inflammasome, marked by the upregulation of NLRP1, NLRP3, AIM2, caspases -1, -3/7, -8, and Gasdermin D (GSDMD), and the release of interleukin-1β (IL-1β) and other cytokines into the vitreous. Similar effects were also detected after 5 weeks of exposure to chronic OHT in an induced glaucoma model. The onset of these immune responses in both spOHT and glaucoma models preceded a 50% deficit in pattern electroretinogram (PERG) amplitude and a significant loss of RGCs 7 days post-injury. The inactivation of inflammasome complexes in Nlrp1−/−, Casp1−/−, and GsdmD−/− knockout animals significantly suppressed the spOHT-induced inflammatory response and protected RGCs. Our results demonstrate that mechanical stress produced by acute repetitive spOHT or chronic OHT is mechanistically linked to inflammasome activation, which leads to RGC dysfunction and death.

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“…Other advantages include simplicity, low costs, parallel analysis of samples, high sample capacity, rapidly obtained results, and possibility ofmultiple detection. [61] The modern HPTLC technique, combined with automated sample application and densitometric scanning, is sensitive and completely reliable, suitable for use in qualitative and quantitative analysis. [62] The acid-dye method can provide a more sensitive technique for certain amines and quaternary ammonium compounds that absorb weakly in the ultraviolet region.…”

Section: Future Aspectsmentioning

confidence: 99%

Analytical methods for venlaflaxine hydrochloride and metabolites determinations in different matrices

Shrivastava¹

2012

Syst Rev Pharm

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A B S T R A C TThere may be significant variation in stereoisomers related to distribution, bioavailability, metabolism, and excretion. Venlafaxine is a bicyclic phenylethylamine derivative, a unique antidepressant,which structurally differs from other currently available anti-depressants. Its mechanism of action is believed to be associated with triggering neurotransmitter activity in the CNS. This drug is a racemic mixture of the (−)-R-enantiomer and (+)-S-enantiomer. O-desmethylvenlaflaxine is the major metabolite formed after first pass metabolism with similar potency as parent drug. Two less potent minor metabolites are N-desmethylvenlafaxine and N,O-didesmethylvenlafaxine. Thus, summarization of all of the analytical methods for the determination of venlaflaxine alone, in combination, or in the presence of other metabolites, is summarized. The keywords used for search were "Analytical methods on Venlaflaxine," "Determination of venlaflaxine," "Determination of venlaflaxine and metabolites," and "Venlaflaxine plasma determinations." Eight spectrophotometry, 26 chromatography, and seven electroanalytical methods were found for the determination of venlaflaxine alone, in formulations, biological matrices, and simultaneous determinations with metabolites and other anti-depressants. Short review of pharmacological activity of venlaflaxine and its metabolites are also presented.

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Spectrophotometric estimation of tamsulosin hydrochloride by acid-dye method

Cited by 11 publications

References 15 publications

Inflammasome-Dependent Dysfunction and Death of Retinal Ganglion Cells after Repetitive Intraocular Pressure Spikes

Inflammasome-Dependent Dysfunction and Death of Retinal Ganglion Cells after Repetitive Intraocular Pressure Spikes

The Inflammasome-Dependent Dysfunction and Death of Retinal Ganglion Cells after Repetitive Intraocular Pressure Spikes

Analytical methods for venlaflaxine hydrochloride and metabolites determinations in different matrices

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