Pub Date : 2018-01-01DOI: 10.4172/2168-975X.1000247
K. GovathiNikhila
Stroke is the second leading cause of death worldwide and the brain damage caused by it can affect communication in several aspects. Voice analysis in dysarthria is challenging because of the complexity of the disorder and its effects on the speech production system. In this study we are presenting a 56-years-old male who was visited to Medanta Hospital with history of hypertension and chief complaint of Right upper limb weakness and slurred speech to the Emergency and later Clinically and Radio logically Diagnosed as LT MCA Infarct. Later, on the day 3 the patient has undergone Speech and Language Evaluation and Diagnosed with Spastic Dysarthria based on Frenched Dysarthria Assessment scale and later a detail Voice Analysis was done with using PRAAT software and analysed voice features. Voice analysis basically deals with decomposition of voice signal into voice parameters for processing the resulted features in desirable application. The features that are extracted in this paper are: frequency, pitch, voice intensity, formant, speech rate and pulse functions like Jitter (local), Jitter (local, absolute), Jitter (rap), Jitter (ppq5), Jitter (ddp), Shimmer (local), Shimmer (local, dB), Shimmer (apq3), Shimmer (apq5), Shimmer (apq11), Shimmer (dda) and Harmonic coefficients. Over all, we conclude with the voice parameters in spastic dysarthria which reveals interesting data on the voice quality with features which helps the clinician for better management. However, large sample study is required.
{"title":"Dysarthrophonia in Association with Voice Analysis: A Case Report","authors":"K. GovathiNikhila","doi":"10.4172/2168-975X.1000247","DOIUrl":"https://doi.org/10.4172/2168-975X.1000247","url":null,"abstract":"Stroke is the second leading cause of death worldwide and the brain damage caused by it can affect communication in several aspects. Voice analysis in dysarthria is challenging because of the complexity of the disorder and its effects on the speech production system. In this study we are presenting a 56-years-old male who was visited to Medanta Hospital with history of hypertension and chief complaint of Right upper limb weakness and slurred speech to the Emergency and later Clinically and Radio logically Diagnosed as LT MCA Infarct. Later, on the day 3 the patient has undergone Speech and Language Evaluation and Diagnosed with Spastic Dysarthria based on Frenched Dysarthria Assessment scale and later a detail Voice Analysis was done with using PRAAT software and analysed voice features. Voice analysis basically deals with decomposition of voice signal into voice parameters for processing the resulted features in desirable application. The features that are extracted in this paper are: frequency, pitch, voice intensity, formant, speech rate and pulse functions like Jitter (local), Jitter (local, absolute), Jitter (rap), Jitter (ppq5), Jitter (ddp), Shimmer (local), Shimmer (local, dB), Shimmer (apq3), Shimmer (apq5), Shimmer (apq11), Shimmer (dda) and Harmonic coefficients. Over all, we conclude with the voice parameters in spastic dysarthria which reveals interesting data on the voice quality with features which helps the clinician for better management. However, large sample study is required.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83820039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-01-01DOI: 10.4172/2168-975X.1000245
H. M. Balkhi, Taseen Gul, S. Sana, E. Haq
1.1 Background: Gliomas are one of the most invasive, highly recurrent, heterogeneous cancers resistant to most of the current treatment regimes and hence almost incurable. CAPE and Dasatinib when used in a congruous combination and durations, present an antitumor potential for glioma. 1.2 Objective: CAPE and Dasatinib in combination have been shown to inhibit proliferation and induce apoptosis in C6 glioma cells. However, the signaling pathway of their antiproliferative and apoptotic effects remains unknown. In this study, the antiproliferative effects of combination treatment on C6 glioma cells were investigated. 1.3 Methods: Expression analysis of proteins thought to be mediating proliferation, cell motility, angiogenesis, and invasion was carried out to delineate the molecular mechanism entailing antineoplastic action of CAPE and Dasatinib. 1.4 Results: Co-treatment induces a change in cellular and nuclear morphology followed by apoptosis and a significant decrease in the activity of catalase and MMP-2, Pro-MMP 2, MMP-9 and Pro-MMP 9 in C6 glioma cells. Moreover, CAPE and Dasatinib modulate the expression of proteins having potential interactive crosstalk with major oncogenic pathways involved in glioma progression. Our results showed that combination treatment modulates the expression of p53, ERK1/2, and AKT in C6 glioma cells. p53, EGFR and PCNA transcript expressions were attuned in co-treated C6 cells. 1.5 Conclusion: Importantly, antineoplastic effects of CAPE and Dasatinib were far greater than those afforded by treatment with a single drug. Together these drugs reduce glioma proliferation and invasion felicitously implying that combination treatment could be a useful therapy for treatment of glioma.
{"title":"Potential Synergism of Caffeic Acid Phenethyl Ester and Dasatinib in C6 Glioma Cell Model: Adumbrating the Molecular Mechanism","authors":"H. M. Balkhi, Taseen Gul, S. Sana, E. Haq","doi":"10.4172/2168-975X.1000245","DOIUrl":"https://doi.org/10.4172/2168-975X.1000245","url":null,"abstract":"1.1 Background: Gliomas are one of the most invasive, highly recurrent, heterogeneous cancers resistant to most of the current treatment regimes and hence almost incurable. CAPE and Dasatinib when used in a congruous combination and durations, present an antitumor potential for glioma. 1.2 Objective: CAPE and Dasatinib in combination have been shown to inhibit proliferation and induce apoptosis in C6 glioma cells. However, the signaling pathway of their antiproliferative and apoptotic effects remains unknown. In this study, the antiproliferative effects of combination treatment on C6 glioma cells were investigated. 1.3 Methods: Expression analysis of proteins thought to be mediating proliferation, cell motility, angiogenesis, and invasion was carried out to delineate the molecular mechanism entailing antineoplastic action of CAPE and Dasatinib. 1.4 Results: Co-treatment induces a change in cellular and nuclear morphology followed by apoptosis and a significant decrease in the activity of catalase and MMP-2, Pro-MMP 2, MMP-9 and Pro-MMP 9 in C6 glioma cells. Moreover, CAPE and Dasatinib modulate the expression of proteins having potential interactive crosstalk with major oncogenic pathways involved in glioma progression. Our results showed that combination treatment modulates the expression of p53, ERK1/2, and AKT in C6 glioma cells. p53, EGFR and PCNA transcript expressions were attuned in co-treated C6 cells. 1.5 Conclusion: Importantly, antineoplastic effects of CAPE and Dasatinib were far greater than those afforded by treatment with a single drug. Together these drugs reduce glioma proliferation and invasion felicitously implying that combination treatment could be a useful therapy for treatment of glioma.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78823698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-01-01DOI: 10.4172/2168-975x.1000249
Bedadyuti Mohanty
Dementia is a clinical situation that requires novel practical dependence based on the dynamic memory failure and subjective loss, as its Latin source proposes: an exit from past mental functioning. The occurrence of dementia ascends with age, making it an undeniably common subject among the matured populace. The nature of manifestations among individuals with dementia is more dependent and helpless, both socially and regarding physical and psychological wellness, introducing advancing difficulties to society and to our medical services and hospitals. In spite of the apparently straightforward premise, the clinical analysis of dementia can be troublesome with de novo functional disability frequently clouded by physical weakness and misery. Clinical and neurotic basis for the fundamental dementia causing illnesses overlaps remarkably. The development of symptoms takes us into the patho-physiological procedure hamper focused on disorder treatment. An incredible number of research activities are in progress to distinguish potential biomarkers of disease prior its occurrence.
{"title":"Dementia: Neuropathology Based on Changes in Tau Protein","authors":"Bedadyuti Mohanty","doi":"10.4172/2168-975x.1000249","DOIUrl":"https://doi.org/10.4172/2168-975x.1000249","url":null,"abstract":"Dementia is a clinical situation that requires novel practical dependence based on the dynamic memory failure and subjective loss, as its Latin source proposes: an exit from past mental functioning. The occurrence of dementia ascends with age, making it an undeniably common subject among the matured populace. The nature of manifestations among individuals with dementia is more dependent and helpless, both socially and regarding physical and psychological wellness, introducing advancing difficulties to society and to our medical services and hospitals. In spite of the apparently straightforward premise, the clinical analysis of dementia can be troublesome with de novo functional disability frequently clouded by physical weakness and misery. Clinical and neurotic basis for the fundamental dementia causing illnesses overlaps remarkably. The development of symptoms takes us into the patho-physiological procedure hamper focused on disorder treatment. An incredible number of research activities are in progress to distinguish potential biomarkers of disease prior its occurrence.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82997939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-01-01DOI: 10.4172/2168-975X.1000243
Caleb T. Epps, M. Allen
Background: Post-concussion syndrome (PCS) occurs in a significant percentage of concussion patients. Functional MRI reveals irregular blood-oxygen level dependent signals in PCS patients. PCS biomarkers with functional predictive values have yet to be discovered and validated. Therefore, this study describes five PCS biomarkers and includes a description of their therapeutic application. Methods: A neurocognitive imaging protocol was developed and a group of healthy control patients was used to generate a normative reference atlas. Biomarker candidate search was performed using an initial sample of PCS patients. Sample validation was applied to each biomarker using a new sample of PCS patients to assess sensitivities/ specificities. A multivariate base rate analysis was performed using 132 new patients and a base rate cutoff matrix was constructed. An example of the biomarker’s therapeutic application in a PCS patient is described. Results: The five functional biomarkers included: Frontal Attentional System hypoactivation, Subcortical System hypoactivation, Visual System hyperactivation, Verbal System hypoactivation, and Frontal/Parietal System hyperactivation. Individual biomarker sensitivities and specificities are reported. Collectively, using the base rate cutoff matrix, a threshold using 3/5 biomarkers below the 10th percentile as the cutoff resulted in a suitable sensitivity (88%) and specificity (99%). The uses of these biomarkers were crucial in guiding the successful treatment of Patient A. Conclusion: We report the discovery of five functional PCS biomarkers. We show an example of the therapeutic application of the five biomarkers in the successful treatment of PCS. These neuroimaging biomarkers serve to advance diagnostic capabilities and subsequent PCS rehabilitation efforts.
{"title":"Discovery of Therapy-targeting Biomarkers for Post-Concussion Syndrome using Functional Neurocognitive Imaging","authors":"Caleb T. Epps, M. Allen","doi":"10.4172/2168-975X.1000243","DOIUrl":"https://doi.org/10.4172/2168-975X.1000243","url":null,"abstract":"Background: Post-concussion syndrome (PCS) occurs in a significant percentage of concussion patients. Functional MRI reveals irregular blood-oxygen level dependent signals in PCS patients. PCS biomarkers with functional predictive values have yet to be discovered and validated. Therefore, this study describes five PCS biomarkers and includes a description of their therapeutic application. Methods: A neurocognitive imaging protocol was developed and a group of healthy control patients was used to generate a normative reference atlas. Biomarker candidate search was performed using an initial sample of PCS patients. Sample validation was applied to each biomarker using a new sample of PCS patients to assess sensitivities/ specificities. A multivariate base rate analysis was performed using 132 new patients and a base rate cutoff matrix was constructed. An example of the biomarker’s therapeutic application in a PCS patient is described. Results: The five functional biomarkers included: Frontal Attentional System hypoactivation, Subcortical System hypoactivation, Visual System hyperactivation, Verbal System hypoactivation, and Frontal/Parietal System hyperactivation. Individual biomarker sensitivities and specificities are reported. Collectively, using the base rate cutoff matrix, a threshold using 3/5 biomarkers below the 10th percentile as the cutoff resulted in a suitable sensitivity (88%) and specificity (99%). The uses of these biomarkers were crucial in guiding the successful treatment of Patient A. Conclusion: We report the discovery of five functional PCS biomarkers. We show an example of the therapeutic application of the five biomarkers in the successful treatment of PCS. These neuroimaging biomarkers serve to advance diagnostic capabilities and subsequent PCS rehabilitation efforts.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83820623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-01-01DOI: 10.4172/2168-975x-c1-020
K. B. Kristensen
{"title":"The future of health outcome measurements of brain disorders","authors":"K. B. Kristensen","doi":"10.4172/2168-975x-c1-020","DOIUrl":"https://doi.org/10.4172/2168-975x-c1-020","url":null,"abstract":"","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75662321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-01-01DOI: 10.4172/2168-975X.1000e127
L. Bergantin
The scientific literature has recently debated (more intensively) the clinical link between Alzheimer ́s disease (AD) and Depression [1]. Despite the accumulation of the amyloid-β (Aβ) in the brain (amyloid cascade hypothesis) has been considered the main issue in the arena of AD, this hypothesis does not explain the fact that there must be changes that may occur during aging process that result in increased production and aggregation of Aβ, thus culminating in the status of AD. Evidences suggest that Ca2+ signalling dysregulation may be such an upstream issue. Environmental issues that prevent amyloid genesis (caloric restriction, cognitive stimulus and antioxidants) virtually restore the neuronal Ca2+ homeostasis, whereas factors that enhance amyloid genesis dysregulate Ca2+ homeostasis. These evidences are supported by experiments which demonstrated that exposure of cultured neurons to Ca2+ ionophores enhances the production of Aβ, as do conditions such as ischemia that cause sustained elevations of Ca2+ concentrations [Ca]c [2]. In addition, considering that the neuron uses Ca2+ signals to regulate the release of neurotransmitter, and that the deficit of neurotransmitter release is causally related to the clinical signs of Depression, then Ca2+ signalling is also one of the main actors in the arena of Depression. Indeed, the monoamine hypothesis of Depression continues to be one actor that dominates the field, which hypothesizes that an imbalance in monoaminergic neurotransmission culminates in the deficit of neurotransmitter release. Despite this hypothesis, pre-clinical and clinical studies have also shown that Depression can lead to cell loss in limbic brain structures, which are critically involved in the status of depression, including the hippocampus [3]. Thus, if Ca2+ signalling dysregulation may be such an upstream issue for AD, then sustained elevations of neuronal [Ca]c may be a reasonable clinical link between AD and Depression, because the sustained elevations of [Ca]c may also lead to neuronal cell death in these structures (limbic brain structures and hippocampus), which are related to the development of Depression.
{"title":"Revisiting the Clinical Link Between Alzheimer's Disease and Depression Through the Ca2+/Camp Signalling Interaction","authors":"L. Bergantin","doi":"10.4172/2168-975X.1000e127","DOIUrl":"https://doi.org/10.4172/2168-975X.1000e127","url":null,"abstract":"The scientific literature has recently debated (more intensively) the clinical link between Alzheimer ́s disease (AD) and Depression [1]. Despite the accumulation of the amyloid-β (Aβ) in the brain (amyloid cascade hypothesis) has been considered the main issue in the arena of AD, this hypothesis does not explain the fact that there must be changes that may occur during aging process that result in increased production and aggregation of Aβ, thus culminating in the status of AD. Evidences suggest that Ca2+ signalling dysregulation may be such an upstream issue. Environmental issues that prevent amyloid genesis (caloric restriction, cognitive stimulus and antioxidants) virtually restore the neuronal Ca2+ homeostasis, whereas factors that enhance amyloid genesis dysregulate Ca2+ homeostasis. These evidences are supported by experiments which demonstrated that exposure of cultured neurons to Ca2+ ionophores enhances the production of Aβ, as do conditions such as ischemia that cause sustained elevations of Ca2+ concentrations [Ca]c [2]. In addition, considering that the neuron uses Ca2+ signals to regulate the release of neurotransmitter, and that the deficit of neurotransmitter release is causally related to the clinical signs of Depression, then Ca2+ signalling is also one of the main actors in the arena of Depression. Indeed, the monoamine hypothesis of Depression continues to be one actor that dominates the field, which hypothesizes that an imbalance in monoaminergic neurotransmission culminates in the deficit of neurotransmitter release. Despite this hypothesis, pre-clinical and clinical studies have also shown that Depression can lead to cell loss in limbic brain structures, which are critically involved in the status of depression, including the hippocampus [3]. Thus, if Ca2+ signalling dysregulation may be such an upstream issue for AD, then sustained elevations of neuronal [Ca]c may be a reasonable clinical link between AD and Depression, because the sustained elevations of [Ca]c may also lead to neuronal cell death in these structures (limbic brain structures and hippocampus), which are related to the development of Depression.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78831411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-01-01DOI: 10.4172/2168-975X.1000250
D. Tavares, D. Moreno, R. Moreno
Introduction: We reviewed the literature to examine: (1) Aspects related to the diagnostic boundaries of mild forms of bipolar disorder (BD); (2) The controversies related to the diagnostic criteria of phasic hypomania and chronic hypomania; (3) Aspects related to the treatment and the use of antidepressants in mild forms of BD. Methods: Comprehensive computer literature search to find relevant peer reviewed articles related to this these topics. Results: Mild forms of BD suffer from the big problem of misdiagnosis with recurrent and treatment resistant major depressive disorder. One factor explaining which explains this, at least in part, is the fact that the current diagnostic criteria for hypomania, as it is concepted today, are is still quite restrictive and often sensitive only to more exuberant clinical pictures, such as mild manias. In addition to this, the use of antidepressants in the mild cases of BD will hardly aid in diagnosis, because strong mood swings are not enough to permit diagnosis (leading to the emergence of hypomania) and are not common in these mild forms. The most important question in the treatment of BD II is not the acute treatment of hypomania itself but the recognition that they exist and influence the recurrence recurrence of depressive episodes. Conclusion: This review showed the fragility and low sensitivity of the current criteria for diagnosis and management of BD II. Clinical trials evaluating the treatment of these conditions cannot be generalizable generalized for all the subpopulation of BD II we see in clinical practice.
{"title":"Heterogeneity in Bipolar II Disorder Treatments: A Literature Review","authors":"D. Tavares, D. Moreno, R. Moreno","doi":"10.4172/2168-975X.1000250","DOIUrl":"https://doi.org/10.4172/2168-975X.1000250","url":null,"abstract":"Introduction: We reviewed the literature to examine: (1) Aspects related to the diagnostic boundaries of mild forms of bipolar disorder (BD); (2) The controversies related to the diagnostic criteria of phasic hypomania and chronic hypomania; (3) Aspects related to the treatment and the use of antidepressants in mild forms of BD. Methods: Comprehensive computer literature search to find relevant peer reviewed articles related to this these topics. Results: Mild forms of BD suffer from the big problem of misdiagnosis with recurrent and treatment resistant major depressive disorder. One factor explaining which explains this, at least in part, is the fact that the current diagnostic criteria for hypomania, as it is concepted today, are is still quite restrictive and often sensitive only to more exuberant clinical pictures, such as mild manias. In addition to this, the use of antidepressants in the mild cases of BD will hardly aid in diagnosis, because strong mood swings are not enough to permit diagnosis (leading to the emergence of hypomania) and are not common in these mild forms. The most important question in the treatment of BD II is not the acute treatment of hypomania itself but the recognition that they exist and influence the recurrence recurrence of depressive episodes. Conclusion: This review showed the fragility and low sensitivity of the current criteria for diagnosis and management of BD II. Clinical trials evaluating the treatment of these conditions cannot be generalizable generalized for all the subpopulation of BD II we see in clinical practice.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88397881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-11-18DOI: 10.4172/2168-975X.1000E125
L. Bergantin
Science is not always linear! Imagine this scenario: The PhD researcher and his supervisor are formulating their experiment. During the experiment course, there is on the bench a residual solution containing Verapamil, an L-type Ca2+ channel blocker (CCB). In a relapse, the PhD researcher decides to add this solution in an isolated smooth muscle preparation. The smooth muscle was prior relaxed with a drug that increased the cAMP cytosolic concentration. According to the classical receptor theory, addition of verapamil in the smooth muscle preparation should enhance the relaxation of the smooth muscle! To his surprise, the PhD researcher observed an incredible contraction of the smooth muscle! Perplexed with this result, the PhD researcher and his supervisor did not know how to explain this phenomenon immediately
{"title":"Neurodegenerative Diseases: Where To Go From Now? Thought Provoking Through Ca2+/cAMP Signaling Interaction","authors":"L. Bergantin","doi":"10.4172/2168-975X.1000E125","DOIUrl":"https://doi.org/10.4172/2168-975X.1000E125","url":null,"abstract":"Science is not always linear! Imagine this scenario: The PhD researcher and his supervisor are formulating their experiment. During the experiment course, there is on the bench a residual solution containing Verapamil, an L-type Ca2+ channel blocker (CCB). In a relapse, the PhD researcher decides to add this solution in an isolated smooth muscle preparation. The smooth muscle was prior relaxed with a drug that increased the cAMP cytosolic concentration. According to the classical receptor theory, addition of verapamil in the smooth muscle preparation should enhance the relaxation of the smooth muscle! To his surprise, the PhD researcher observed an incredible contraction of the smooth muscle! Perplexed with this result, the PhD researcher and his supervisor did not know how to explain this phenomenon immediately","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91093123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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