Metabolism of valine chirally labeled with carbon 13 and deuterium in vitamin B12-folate-deficient rats in vivo. Studies on the physiological role of keto-enol tautomerization.

In addition to the metabolic role of vitamin D, which is well known and clearly defined, there have been many hypotheses regarding its anti-proliferative and pro-apoptotic role. Epidemiology and Significance of Prostate Cancer. Prostate cancer is the second most common malignancy in men. Long period of cancerogenesis, available tumor markers and high incidence make this cancer ideal for preventive measures. Physiological Role of Vitamin D and its Effect on Prostate Cancer Cells. In vitro and in vivo studies have shown the anti-proliferative and pro-apoptopic role of vitamin D. Disorders of vitamin D metabolism are noted in vitamin D gene level, vitamin D receptor, vitamin D responsive elements and androgen receptors. We present the most important effect of those changes on vitamin D metabolism. Conclusion. Available studies on vitamin D level in serum, prostate tissue, observed activity of vitamin D enzymes and genetic changes give us only a slight insight into the basic mechanisms of vitamin D action in the development of prostate cancer; therefore, further investigations are needed.

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Hering-Breuer Reflex and pre-Botzinger Complex: A Literature Survey

Journal of Bangladesh Society of Physiologist ◽

10.3329/jbsp.v2i0.988 ◽

1970 ◽

Vol 2 ◽

pp. 89-94

Author(s):

M Ahmed

Keyword(s):

Human Subjects ◽

Respiratory Rhythm ◽

Physiological Role ◽

Personal Communication ◽

In Vivo Studies ◽

Respiratory Rhythmogenesis ◽

Neuronal Regulation ◽

Bötzinger Complex

The existence and physiological role of Hering-Breuer reflex and pre-Botzinger complex has long been depreciated by the Bangladesh society of physiologist (personal communication). The aim of this mini review is to highlight the recent findings on the aforementioned topics. Due to the difficulties in vivo studies in human subjects, many aspects of the neuronal regulation of the respiratory rhythm are still unclear. However, the recent localization of the pre-Botzinger complex in humans and advances in technologies necessitates further exploration of the neuronal circuits in the pre-BotC complex which will subsequently unwrap the magical box and pave the way to solve the puzzle of the mechanism of respiratory rhythmogenesis and its modulation in different pathophysiological conditions. Key Words: Physiology; Hering-Breuer reflex; pre-Botzinger complex; Rhythmic respiration DOI:10.3329/jbsp.v2i0.988 J Bangladesh Soc Physiol. 2007 Dec;(2):89-94.

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Role of mesangial cell in glomerular response to volume and angiotensin II

AJP Renal Physiology ◽

10.1152/ajprenal.1993.264.1.f158 ◽

1993 ◽

Vol 264 (1) ◽

pp. F158-F165 ◽

Cited By ~ 4

Author(s):

R. C. Blantz ◽

F. B. Gabbai ◽

B. J. Tucker ◽

T. Yamamoto ◽

C. B. Wilson

Keyword(s):

Angiotensin Ii ◽

Hydrostatic Pressure ◽

Mesangial Cell ◽

Physiological Role ◽

In Vivo Studies ◽

Ang Ii ◽

Plasma Volume Expansion ◽

Single Nephron

We have examined the physiological role of the mesangial cell in the regulation of glomerular hemodynamics utilizing mesangial cell lysis by the administration of antithymocyte antibody serum (ATS) 24 h before micropuncture evaluation. Plasma volume expansion (PVE) in normal NaCl-depleted rats increased single-nephron glomerular filtration rate (SNGFR) by 30% because of increases in single-nephron plasma flow (SNPF), whereas glomerular capillary hydrostatic pressure (PG) remained constant. SNGFR did not increase with PVE in NaCl-depleted ATS rats despite increases in SNPF, and PG increased significantly (51 +/- 2 to 67 +/- 3 mmHg) because of afferent arteriolar dilation, whereas efferent resistance remained elevated. Angiotensin II (ANG II) infusion in normal rats decreased SNGFR because of reductions in SNPF and the glomerular ultrafiltration coefficient (LpA), whereas the hydrostatic pressure gradient (delta P) increased. In ATS rats ANG II infusion did not change SNGFR, LpA, or delta P. These in vivo studies suggest that the mesangial cell plays an important role in the regulation of LpA, efferent arteriolar resistance, and the regulation of PG, whereas this cell exerts little effect on the afferent arteriole.

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APPsα rescues impaired Ca2+ homeostasis in APP- and APLP2-deficient hippocampal neurons

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.2011506118 ◽

2021 ◽

Vol 118 (26) ◽

pp. e2011506118

Author(s):

Susann Ludewig ◽

Ulrike Herrmann ◽

Kristin Michaelsen-Preusse ◽

Kristin Metzdorf ◽

Jennifer Just ◽

...

Keyword(s):

Synaptic Plasticity ◽

Hippocampal Neurons ◽

Therapeutic Potential ◽

Amyloid Β ◽

Physiological Role ◽

In Vivo Studies ◽

Associated Proteins

Alterations in Ca2+ homeostasis have been reported in several in vitro and in vivo studies using mice expressing the Alzheimer’s disease–associated transgenes, presenilin and the amyloid precursor protein (APP). While intense research focused on amyloid-β–mediated functions on neuronal Ca2+ handling, the physiological role of APP and its close homolog APLP2 is still not fully clarified. We now elucidate a mechanism to show how APP and its homolog APLP2 control neuronal Ca2+ handling and identify especially the ectodomain APPsα as an essential regulator of Ca2+ homeostasis. Importantly, we demonstrate that the loss of APP and APLP2, but not APLP2 alone, impairs Ca2+ handling, the refill of the endoplasmic reticulum Ca2+ stores, and synaptic plasticity due to altered function and expression of the SERCA-ATPase and expression of store-operated Ca2+ channel–associated proteins Stim1 and Stim2. Long-term AAV-mediated expression of APPsα, but not acute application of the recombinant protein, restored physiological Ca2+ homeostasis and synaptic plasticity in APP/APLP2 cDKO cultures. Overall, our analysis reveals an essential role of the APP family and especially of the ectodomain APPsα in Ca2+ homeostasis, thereby highlighting its therapeutic potential.

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Magnesium Chloride is an Effective Therapeutic Agent for Prostate Cancer

Functional Foods in Health and Disease ◽

10.31989/ffhd.v8i1.368 ◽

2018 ◽

Vol 8 (1) ◽

pp. 62 ◽

Cited By ~ 2

Author(s):

Julianna Maria Santos ◽

Fazle Hussain

Keyword(s):

Prostate Cancer ◽

Magnesium Chloride ◽

Epithelial Mesenchymal Transition ◽

Chromatin Condensation ◽

Myosin Ii ◽

In Vivo Studies ◽

Migration Speed ◽

Mesenchymal Transition

Background: Reduced levels of magnesium can cause several diseases and increase cancer risk. Motivated by magnesium chloride’s (MgCl2) non-toxicity, physiological importance, and beneficial clinical applications, we studied its action mechanism and possible mechanical, molecular, and physiological effects in prostate cancer with different metastatic potentials.Methods: We examined the effects of MgCl2, after 24 and 48 hours, on apoptosis, cell migration, expression of epithelial mesenchymal transition (EMT) markers, and V-H+-ATPase, myosin II (NMII) and the transcription factor NF Kappa B (NFkB) expressions.Results: MgCl2 induces apoptosis, and significantly decreases migration speed in cancer cells with different metastatic potentials. MgCl2 reduces the expression of V-H+-ATPase and myosin II that facilitates invasion and metastasis, suppresses the expression of vimentin and increases expression of E-cadherin, suggesting a role of MgCl2 in reversing the EMT. MgCl2 also significantly increases the chromatin condensation and decreases NFkB expression.Conclusions: These results suggest a promising preventive and therapeutic role of MgCl2 for prostate cancer. Further studies should explore extending MgCl2 therapy to in vivo studies and other cancer types.Keywords: Magnesium chloride, prostate cancer, migration speed, V-H+-ATPase, and EMT.

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The role of anti-endothelial cell antibodies in Kawasaki disease -in vitro and in vivo studies

Clinical & Experimental Immunology ◽

10.1046/j.1365-2249.2002.02000.x ◽

2002 ◽

Vol 130 (2) ◽

pp. 233-240 ◽

Cited By ~ 50

Author(s):

E. GRUNEBAUM ◽

M. BLANK ◽

S. COHEN ◽

A. AFEK ◽

J. KOPOLOVIC ◽

...

Keyword(s):

Endothelial Cell ◽

Kawasaki Disease ◽

In Vivo Studies

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Potential Role of Birds in Japanese Encephalitis Virus Zoonotic Transmission and Genotype Shift

Viruses ◽

10.3390/v13030357 ◽

2021 ◽

Vol 13 (3) ◽

pp. 357

Author(s):

Muddassar Hameed ◽

Abdul Wahaab ◽

Mohsin Nawaz ◽

Sawar Khan ◽

Jawad Nazir ◽

...

Keyword(s):

Japanese Encephalitis Virus ◽

Japanese Encephalitis ◽

Encephalitis Virus ◽

Zoonotic Transmission ◽

In Vivo Studies ◽

Genotype I ◽

Genotype Iii

Japanese encephalitis (JE) is a vaccine-preventable disease caused by the Japanese encephalitis virus (JEV), which is primarily prevalent in Asia. JEV is a Flavivirus, classified into a single serotype with five genetically distinct genotypes (I, II, III, IV, and V). JEV genotype III (GIII) had been the most dominant strain and caused numerous outbreaks in the JEV endemic countries until 1990. However, recent data shows the emergence of JEV genotype I (GI) as a dominant genotype and it is gradually displacing GIII. The exact mechanism of this genotype displacement is still unclear. The virus can replicate in mosquito vectors and vertebrate hosts to maintain its zoonotic life cycle; pigs and aquatic wading birds act as an amplifying/reservoir hosts, and the humans and equines are dead-end hosts. The important role of pigs as an amplifying host for the JEV is well known. However, the influence of other domestic animals, especially birds, that live in high abundance and close proximity to the human is not well studied. Here, we strive to briefly highlight the role of birds in the JEV zoonotic transmission, discovery of birds as a natural reservoirs and amplifying host for JEV, species of birds susceptible to the JEV infection, and the proposed effect of JEV on the poultry industry in the future, a perspective that has been neglected for a long time. We also discuss the recent in vitro and in vivo studies that show that the newly emerged GI viruses replicated more efficiently in bird-derived cells and ducklings/chicks than GIII, and an important role of birds in the JEV genotype shift from GIII to GI.

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The Novel Role of PGC1α in Bone Metabolism

International Journal of Molecular Sciences ◽

10.3390/ijms22094670 ◽

2021 ◽

Vol 22 (9) ◽

pp. 4670

Author(s):

Cinzia Buccoliero ◽

Manuela Dicarlo ◽

Patrizia Pignataro ◽

Francesco Gaccione ◽

Silvia Colucci ◽

...

Keyword(s):

Bone Metabolism ◽

Osteoblastic Differentiation ◽

In Vivo Studies ◽

Peroxisome Proliferator ◽

Sirtuin 3 ◽

Peroxisome Proliferator Activated Receptor ◽

Increased Risk

Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) is a protein that promotes transcription of numerous genes, particularly those responsible for the regulation of mitochondrial biogenesis. Evidence for a key role of PGC1α in bone metabolism is very recent. In vivo studies showed that PGC1α deletion negatively affects cortical thickness, trabecular organization and resistance to flexion, resulting in increased risk of fracture. Furthermore, in a mouse model of bone disease, PGC1α activation stimulates osteoblastic gene expression and inhibits atrogene transcription. PGC1α overexpression positively affects the activity of Sirtuin 3, a mitochondrial nicotinammide adenina dinucleotide (NAD)-dependent deacetylase, on osteoblastic differentiation. In vitro, PGC1α overexpression prevents the reduction of mitochondrial density, membrane potential and alkaline phosphatase activity caused by Sirtuin 3 knockdown in osteoblasts. Moreover, PGC1α influences the commitment of skeletal stem cells towards an osteogenic lineage, while negatively affects marrow adipose tissue accumulation. In this review, we will focus on recent findings about PGC1α action on bone metabolism, in vivo and in vitro, and in pathologies that cause bone loss, such as osteoporosis and type 2 diabetes.

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Novel Insights on the Role of Nitric Oxide in the Ovary: A Review of the Literature

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph18030980 ◽

2021 ◽

Vol 18 (3) ◽

pp. 980

Author(s):

Maria Cristina Budani ◽

Gian Mario Tiboni

Keyword(s):

Nitric Oxide ◽

In Vivo Studies ◽

Published Data ◽

Vitro Fertilization ◽

Peripheral Neurons ◽

Relevant Role ◽

Oocyte Meiotic Maturation

Nitric oxide (NO) is formed during the oxidation of L-arginine to L-citrulline by the action of multiple isoenzymes of NO synthase (NOS): neuronal NOS (nNOS), endotelial NOS (eNOS), and inducible NOS (iNOS). NO plays a relevant role in the vascular endothelium, in central and peripheral neurons, and in immunity and inflammatory systems. In addition, several authors showed a consistent contribution of NO to different aspects of the reproductive physiology. The aim of the present review is to analyse the published data on the role of NO within the ovary. It has been demonstrated that the multiple isoenzymes of NOS are expressed and localized in the ovary of different species. More to the point, a consistent role was ascribed to NO in the processes of steroidogenesis, folliculogenesis, and oocyte meiotic maturation in in vitro and in vivo studies using animal models. Unfortunately, there are few nitric oxide data for humans; there are preliminary data on the implication of nitric oxide for oocyte/embryo quality and in-vitro fertilization/embryo transfer (IVF/ET) parameters. NO plays a remarkable role in the ovary, but more investigation is needed, in particular in the context of human ovarian physiology.

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