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Article ; Online: Elevated Protein Kinase A Activity in Stomach Mesenchyme Disrupts Mesenchymal-epithelial Crosstalk and Induces Preneoplasia.

Puri, Pawan / Grimmett, Garfield / Faraj, Rawah / Gibson, Laurielle / Gilbreath, Ebony / Yoder, Bradley K

Cellular and molecular gastroenterology and hepatology

2022 Volume 14, Issue 3, Page(s) 643–668.e1

Abstract: Background & aims: Mesenchymal-epithelial crosstalk (MEC) in the stomach is executed by pathways such as bone morphogenetic protein (BMP) and extracellular signal-regulated kinase (ERK). Mis-regulation of MEC disrupts gastric homeostasis and causes ... ...

Abstract	Background & aims: Mesenchymal-epithelial crosstalk (MEC) in the stomach is executed by pathways such as bone morphogenetic protein (BMP) and extracellular signal-regulated kinase (ERK). Mis-regulation of MEC disrupts gastric homeostasis and causes tumorigenesis. Protein Kinase A (PKA) crosstalks with BMP and ERK signaling; however, PKA function(s) in stomach development and homeostasis remains undefined. Methods: We generated a novel Six2-Cre Results: Lineage tracing showed that Six2-Cre activity in the stomach is restricted to the mesenchymal compartment. CA-PKA mice showed disruption of gastric homeostasis characterized by aberrant mucosal development and epithelial hyperproliferation; ultimately developing multiple features of gastric corpus preneoplasia including decreased parietal cells, mucous cell hyperplasia, spasmolytic peptide expressing metaplasia with intestinal characteristics, and dysplastic and invasive cystic glands. Furthermore, mutant corpus showed marked chronic inflammation characterized by infiltration of lymphocytes and myeloid-derived suppressor cells along with the upregulation of innate and adaptive immune system components. Striking upregulation of inflammatory mediators and STAT3 activation was observed. Mechanistically, we determined there is an activation of ERK1/2 and downregulation of BMP/SMAD signaling characterized by marked upregulation of BMP inhibitor gremlin 1. Conclusions: We report a novel role of PKA signaling in gastric MEC execution and show that PKA activation in the gastric mesenchyme drives preneoplasia by creating a proinflammatory and proproliferative microenvironment associated with the downregulation of BMP/SMAD signaling and activation of ERK1/2.
MeSH term(s)	Animals ; Bone Morphogenetic Proteins/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Gastric Mucosa/pathology ; Mesoderm/metabolism ; Mice ; Stomach
Chemical Substances	Bone Morphogenetic Proteins ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
Language	English
Publishing date	2022-06-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2819778-1
ISSN	2352-345X ; 2352-345X
ISSN (online)	2352-345X
ISSN	2352-345X
DOI	10.1016/j.jcmgh.2022.06.001
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Article ; Online: Molecular characterization of nephron progenitors and their early epithelial derivative structures in the nephrogenic zone of the canine fetal kidney

Rawah Faraj / Angela Irizarry-Alfonzo / Pawan Puri

European Journal of Histochemistry, Vol 63, Iss

2019 Volume 3

Abstract: Nephron progenitors (NPs) and nephrogenesis have been extensively studied in mice and humans and have provided insights into the mechanisms of renal development, disease and possibility of NP-based therapies. However, molecular features of NPs and their ... ...

Abstract	Nephron progenitors (NPs) and nephrogenesis have been extensively studied in mice and humans and have provided insights into the mechanisms of renal development, disease and possibility of NP-based therapies. However, molecular features of NPs and their derivatives in the canine fetal kidney (CFK) remain unknown. This study was focused to characterize the expression of potential markers of canine NPs and their derivatives by immuno-fluorescence and western blot analysis. Transcription factors (TFs) SIX1 and SIX2, well-characterized human NP markers, were expressed in NPs surrounding the ureteric bud in the CFK. Canine NPs also expressed ITGA8 and NCAM1, surface markers previously used to isolate NPs from the mouse and human fetal kidneys. TF, PAX2 was detected in the ureteric bud, NPs and their derivative structures such as renal vesicle and S-shaped body. This study highlights the similarities in dog, mouse and human renal development and characterizes markers to identify canine NPs and their derivatives. These results will facilitate the isolation of canine NPs and their functional characterization to develop NP-based therapies for canine renal diseases.
Keywords	Nephron progenitor ; renal development ; nephrogenesis ; Biology (General) ; QH301-705.5
Subject code	630
Language	English
Publishing date	2019-09-01T00:00:00Z
Publisher	PAGEPress Publications
Document type	Article ; Online
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Article ; Online: Molecular characterization of nephron progenitors and their early epithelial derivative structures in the nephrogenic zone of the canine fetal kidney.

Faraj, Rawah / Irizarry-Alfonzo, Angela / Puri, Pawan

European journal of histochemistry : EJH

2019 Volume 63, Issue 3

Abstract	Nephron progenitors (NPs) and nephrogenesis have been extensively studied in mice and humans and have provided insights into the mechanisms of renal development, disease and possibility of NP-based therapies. However, molecular features of NPs and their derivatives in the canine fetal kidney (CFK) remain unknown. This study was focused to characterize the expression of potential markers of canine NPs and their derivatives by immuno-fluorescence and western blot analysis. Transcription factors (TFs) SIX1 and SIX2, well-characterized human NP markers, were expressed in NPs surrounding the ureteric bud in the CFK. Canine NPs also expressed ITGA8 and NCAM1, surface markers previously used to isolate NPs from the mouse and human fetal kidneys. TF, PAX2 was detected in the ureteric bud, NPs and their derivative structures such as renal vesicle and S-shaped body. This study highlights the similarities in dog, mouse and human renal development and characterizes markers to identify canine NPs and their derivatives. These results will facilitate the isolation of canine NPs and their functional characterization to develop NP-based therapies for canine renal diseases.
MeSH term(s)	Animals ; Biomarkers/metabolism ; Blotting, Western ; Dogs/embryology ; Epithelial Cells/cytology ; Epithelial Cells/metabolism ; Female ; Fluorescent Antibody Technique ; Nephrons/cytology ; Nephrons/metabolism ; Pregnancy ; Transcription Factors/metabolism
Chemical Substances	Biomarkers ; Transcription Factors
Language	English
Publishing date	2019-09-23
Publishing country	Italy
Document type	Journal Article
ZDB-ID	1109511-8
ISSN	2038-8306 ; 0391-7258 ; 1121-4201 ; 1121-760X
ISSN (online)	2038-8306
ISSN	0391-7258 ; 1121-4201 ; 1121-760X
DOI	10.4081/ejh.2019.3049
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Article ; Online: Lipid Profile and C-Reactive Protein Levels in Healthy, Overweight and Obese Adults

Vaneet Kaur / Himanshu Madaan / Meenakshi Puri / Pawan Kumar Kare

Journal of Clinical and Diagnostic Research, Vol 14, Iss 4, Pp BC01-BC

A Hospital-based Observational Study

2020 Volume 04

Abstract: Introduction: Numerous biomarkers involved in inflammation have been associated with cardiovascular events, out of which high sensitivity-C-Reactive Protein (hs-CRP), an acute-phase protein, appears to be the most promising. The association between ... ...

Abstract	Introduction: Numerous biomarkers involved in inflammation have been associated with cardiovascular events, out of which high sensitivity-C-Reactive Protein (hs-CRP), an acute-phase protein, appears to be the most promising. The association between dyslipidaemia and obesity is well established in literature and has been found to be risk factor for Cardiovascular Disease (CVD). Aim: To study the levels of lipid profile and hs-CRP and also find out the relationship between hs-CRP and Body Mass Index (BMI) in obesity. Materials and Methods: The present observational study was carried out from June 2018 to August 2018 in Kalpana Chawla Government Medical College, Haryana, India. A total of 100 apparently healthy volunteers, aged 21-60 years were enrolled for this study. The participants were divided on the basis of BMI into three groups; Healthy (normal): 18.5-22.9 kg/m2, overweight: 23-24.9 kg/m2, and obese ≥25 kg/m2. Anthropometric measurements and biochemical investigations were conceded in all the study participants. Lipid profile and hs-CRP levels were estimated on fully automated clinical chemistry analyser. Statistical analysis was conducted using IBM SPSS statistics (version 22.0). A p<0.05 was considered as significant level. Results: The median levels of HDL were the lowest in the obese group and a statistically significant difference was observed in HDL levels between healthy and obese group (z=3.190, p=0.001) and between overweight and obese group (z=2.760, p=0.006). The median hs-CRP levels were highest in the obese group and statistically significant difference was observed between healthy and overweight group (z=2.009, p=0.044) and between healthy and obese group (z=2.849, p=0.004). A significant positive correlation was observed between BMI and hs-CRP levels (r=0.302, p<0.002). It was further observed that 17 subjects of obese group had hs-CRP levels greater than 3 mg/L as compared to eight of healthy group and nine of overweight group. Conclusion: The subjects of the obese group are at the ...
Keywords	acute phase protein ; body mass index ; cardiovascular disease ; Medicine ; R
Subject code	796
Language	English
Publishing date	2020-04-01T00:00:00Z
Publisher	JCDR Research and Publications Private Limited
Document type	Article ; Online
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Article ; Online: The regulation of male fertility by the PTPN11 tyrosine phosphatase.

Puri, Pawan / Walker, William H

Seminars in cell & developmental biology

2016 Volume 59, Page(s) 27–34

Abstract: PTPN11 (also known as SHP2) is a ubiquitously expressed non-receptor tyrosine phosphatase that regulates cell survival, proliferation, differentiation, migration and adhesion. Naturally occurring mutations in the PTPN11 gene cause Noonan and LEOPARD ... ...

Abstract	PTPN11 (also known as SHP2) is a ubiquitously expressed non-receptor tyrosine phosphatase that regulates cell survival, proliferation, differentiation, migration and adhesion. Naturally occurring mutations in the PTPN11 gene cause Noonan and LEOPARD syndromes, two genetic disorders that are characterized by a spectrum of defects including male infertility. This review summarizes four cellular and molecular mechanisms by which PTPN11 acts to support male fertility. First, PTPN11 is required for the proliferation and survival of spermatogonial stem cells (SSCs) that are essential to replenish the germ cells that will become sperm. Second, PTPN11 regulation of cellular adhesion functions in Sertoli cells is required to maintain the blood-testis barrier (BTB) that protects meiotic and post-meiotic germ cells. Third, expression of PTPN11 in Sertoli cells is essential to prevent premature differentiation and exhaustion of the SSC population and to maintain the SSC niche. Finally, in Leydig cells, PTPN11 supports mitochondrial fusion and the expression of acyl-CoA synthetase (ACSL4) needed for the production of steroids including testosterone, which is required for fertility.
Language	English
Publishing date	2016-11
Publishing country	England
Document type	Review ; Journal Article
ZDB-ID	1312473-0
ISSN	1096-3634 ; 1084-9521
ISSN (online)	1096-3634
ISSN	1084-9521
DOI	10.1016/j.semcdb.2016.01.020
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Zs.A 2918: Show issues

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Article: A multicentre, double-blind, placebo-controlled randomized trial of Mycobacterium w in critically ill patients with COVID-19 (ARMY-2).

Sehgal, Inderpaul S / Agarwal, Ritesh / Jindal, Atul / Siddiqui, Md Sabah / Mohan, Anant / Pal, Arnab / Guleria, Randeep / Bhalla, Ashish / Kajal, Kamal / Malhotra, Pankaj / Puri, Goverdhan Dutt / Khadanga, Sagar / Joshi, Rajnish / Singh, Sarman / Saigal, Saurabh / Nagarkar, Nitin M / Suri, Vikas / Bhatnagar, Sushma / Tiwari, Pawan /

Singh, Mini P / Yaddanapudi, Laxmi Narayana / Mittal, Saurabh / Chauhan, Anshika / Banerjee, Gaurab / Rai, Deependra K / Gupta, Bikram K

Lung India : official organ of Indian Chest Society

2024 Volume 41, Issue 2, Page(s) 84–92

Abstract: Background: Mycobacterium w (Mw), an immunomodulator, resulted in better clinical status in severe coronavirus infectious disease 19 (COVID-19) but no survival benefit in a previous study. Herein, we investigate whether Mw could improve clinical ... ...

Abstract	Background: Mycobacterium w (Mw), an immunomodulator, resulted in better clinical status in severe coronavirus infectious disease 19 (COVID-19) but no survival benefit in a previous study. Herein, we investigate whether Mw could improve clinical outcomes and survival in COVID-19. Materials and methods: In a multicentric, randomized, double-blind, parallel-group, placebo-controlled trial, we randomized hospitalized subjects with severe COVID-19 to receive either 0.3 mL/day of Mw intradermally or a matching placebo for three consecutive days. The primary outcome was 28-day mortality. The co-primary outcome was the distribution of clinical status assessed on a seven-point ordinal scale ranging from discharged (category 1) to death (category 7) on study days 14, 21, and 28. The key secondary outcomes were the change in sequential organ failure assessment (SOFA) score on days 7 and 14 compared to the baseline, treatment-emergent adverse events, and others. Results: We included 273 subjects (136 Mw, 137 placebo). The use of Mw did not improve 28-day survival (Mw vs. placebo, 18 [13.2%] vs. 12 [8.8%], P = 0.259) or the clinical status on days 14 (odds ratio [OR], 1.33; 95% confidence intervals [CI], 0.79-2.3), 21 (OR, 1.49; 95% CI, 0.83-2.7) or 28 (OR, 1.49; 95% CI, 0.79-2.8) between the two study arms. There was no difference in the delta SOFA score or other secondary outcomes between the two groups. We observed higher injection site reactions with Mw. Conclusion: Mw did not reduce 28-day mortality or improve clinical status on days 14, 21 and 28 compared to placebo in patients with severe COVID-19. [Trial identifier: CTRI/2020/04/024846].
Language	English
Publishing date	2024-02-27
Publishing country	India
Document type	Journal Article
ZDB-ID	2410801-7
ISSN	0974-598X ; 0970-2113
ISSN (online)	0974-598X
ISSN	0970-2113
DOI	10.4103/lungindia.lungindia_426_23
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Article ; Online: The tyrosine phosphatase SHP2 regulates Sertoli cell junction complexes.

Puri, Pawan / Walker, William H

Biology of reproduction

2013 Volume 88, Issue 3, Page(s) 59

Abstract: The blood-testis barrier (BTB) is a large junctional complex composed of tight junctions, adherens junctions, and gap junctions between adjacent Sertoli cells in the seminiferous tubules of the testis. Maintenance of the BTB as well as the controlled ... ...

Abstract	The blood-testis barrier (BTB) is a large junctional complex composed of tight junctions, adherens junctions, and gap junctions between adjacent Sertoli cells in the seminiferous tubules of the testis. Maintenance of the BTB as well as the controlled disruption and reformation of the barrier is essential for spermatogenesis and male fertility. Tyrosine phosphorylation of BTB proteins is known to regulate the integrity of adherens and tight junctions found at the BTB. SHP2 is a nonreceptor protein tyrosine phosphatase (PTP) and a key regulator of growth factor-mediated tyrosine kinase signaling pathways. We found that SHP2 is localized to Sertoli-Sertoli cell junctions in rat testis. The overexpression of a constitutive active SHP2 mutant, SHP2 Q79R, up-regulated the BTB disruptor ERK1/2 via Src kinase in primary rat Sertoli cells in culture. Furthermore, focal adhesion kinase (FAK), which also supports BTB integrity, was found to interact with SHP2 and constitutive activation of SHP2 decreased FAK tyrosine phosphorylation. Expression of the SHP2 Q79R mutant in primary cultured Sertoli cells also resulted in the loss of tight junction and adherens junction integrity that corresponded with the disruption of the actin cytoskeleton and mislocalization of adherens junction and tight junction proteins N-cadherin, β-catenin, and ZO-1 away from the plasma membrane. These results suggest that SHP2 is a key regulator of BTB integrity and Sertoli cell support of spermatogenesis and fertility.
MeSH term(s)	Animals ; Blood-Testis Barrier/metabolism ; Focal Adhesion Protein-Tyrosine Kinases/metabolism ; Hepatocyte Growth Factor/metabolism ; Intercellular Junctions/metabolism ; Male ; Mitogen-Activated Protein Kinases/metabolism ; Protein Tyrosine Phosphatase, Non-Receptor Type 11/metabolism ; Rats ; Rats, Sprague-Dawley ; Sertoli Cells/enzymology
Chemical Substances	Hepatocyte Growth Factor (67256-21-7) ; Focal Adhesion Protein-Tyrosine Kinases (EC 2.7.10.2) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 (EC 3.1.3.48)
Language	English
Publishing date	2013-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1118-6
ISSN	1529-7268 ; 0006-3363
ISSN (online)	1529-7268
ISSN	0006-3363
DOI	10.1095/biolreprod.112.104414
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Zs.A 551: Show issues

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Article ; Online: Six2creFrs2α knockout mice are a novel model of renal cystogenesis.

Puri, Pawan / Bushnell, Daniel / Schaefer, Caitlin M / Bates, Carlton M

Scientific reports

2016 Volume 6, Page(s) 36736

Abstract: Six2cre-mediated deletion of Frs2α (Six2creFrs2αKO), a major fibroblast growth factor receptor (Fgfr) docking protein in mouse nephron progenitors results in perinatal renal hypoplasia; however, postnatal Six2creFrs2αKO kidneys develop cysts. We sought ... ...

Abstract	Six2cre-mediated deletion of Frs2α (Six2creFrs2αKO), a major fibroblast growth factor receptor (Fgfr) docking protein in mouse nephron progenitors results in perinatal renal hypoplasia; however, postnatal Six2creFrs2αKO kidneys develop cysts. We sought to determine the pathogenesis of Six2creFrs2αKO cyst formation. We performed histological assays, Western blots, and quantitative PCR (qPCR). While embryonic day (E) 18.5 Six2Frs2αKO kidneys were hypoplastic and not cystic, postnatal day (P) 7 mutants had proximal tubular-derived cysts that nearly replaced the renal parenchyma by P21. Mutants had high proximal tubular proliferation rates and interstitial fibrosis, similar to known polycystic kidney disease (PKD) models. Six2creFrs2αKO kidneys also had upregulation of Wnt/βcatenin signaling, macrophage infiltration and chemokine production (e.g. ectopic Ccl2 in non-dilated proximal tubules), and augmented hedgehog signaling, features also seen in other PKD models. We saw increased Gli1 (hedgehog readout) in postnatal Six2creFrs2αKO interstitium and ectopic sonic hedgehog (Shh) in subsets of non-dilated P7 mutant proximal tubules (likely driving the stromal Gli expression). As ectopic tubular Shh and Ccl2 expression is seen after acute kidney injury (AKI), we interrogated another bone fide AKI marker, Kim1 and noted ectopic expression in P7 non-dilated proximal tubules. These observations suggest that aberrantly activated "AKI" pathways may drive pathogenesis in PKD.
MeSH term(s)	Animals ; Apoptosis ; Blood Urea Nitrogen ; Cell Proliferation ; Chemokines/metabolism ; Fibrosis/metabolism ; Gene Expression Regulation ; Hedgehog Proteins/metabolism ; Hepatitis A Virus Cellular Receptor 1/genetics ; Hepatitis A Virus Cellular Receptor 1/metabolism ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Inflammation ; Kidney/embryology ; Kidney/growth & development ; Kidney/metabolism ; Kidney Tubules/metabolism ; Macrophages/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Mutation ; Polycystic Kidney Diseases/genetics ; Polycystic Kidney Diseases/metabolism ; Real-Time Polymerase Chain Reaction ; Signal Transduction ; Time Factors ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Zinc Finger Protein GLI1/metabolism ; beta Catenin/metabolism
Chemical Substances	Chemokines ; FRS2alpha protein, mouse ; Gli protein, mouse ; Havcr1 protein, mouse ; Hedgehog Proteins ; Hepatitis A Virus Cellular Receptor 1 ; Homeodomain Proteins ; Membrane Proteins ; Shh protein, mouse ; Six2 protein, mouse ; Transcription Factors ; Zinc Finger Protein GLI1 ; beta Catenin
Language	English
Publishing date	2016--17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep36736
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Article ; Online: Post-implementation Review of the Himalaya Home Care Project for Home Isolated COVID-19 Patients in Nepal.

Amatya, Rakchya / Mishra, Kritika / Karki, Kshitij / Puri, Isha / Gautam, Archita / Thapa, Sweta / Katwal, Urmila / Veer, Siddhesh / Zervos, John / Kaljee, Linda / Prentiss, Tyler / Zenlea, Kate / Maki, Gina / Rayamajhi, Pawan Jung / Khanal, Narendra K / Thapa, Pomawati / Upadhyaya, Madan Kumar / Bajracharya, Deepak

Frontiers in public health

2022 Volume 10, Page(s) 891611

Abstract: Background: The emergence of coronavirus disease 2019 (COVID-19) has resulted in a pandemic that has significantly impacted healthcare systems at a global level. Health care facilities in Nepal, as in other low- and middle-income countries, have limited ...

Abstract	Background: The emergence of coronavirus disease 2019 (COVID-19) has resulted in a pandemic that has significantly impacted healthcare systems at a global level. Health care facilities in Nepal, as in other low- and middle-income countries, have limited resources for the treatment and management of COVID-19 patients. Only critical cases are admitted to the hospital resulting in most patients in home isolation. Methods: Himalaya Home Care (HHC) was initiated to monitor and provide counseling to home isolated COVID-19 patients for disease prevention, control, and treatment. Counselors included one physician and four nurses. Lists of patients were obtained from district and municipal health facilities. HHC counselors called patients to provide basic counseling services. A follow-up check-in phone call was conducted 10 days later. During this second call, patients were asked about their perceptions of the HHC program. Project objects were: (1) To support treatment of home isolated persons with mild to moderate COVID-19, decrease burden of hospitalizations, and decrease risks for disease transmission; and, (2) To improve the health status of marginalized, remote, and vulnerable populations in Nepal during the COVID-19 pandemic. Results: Data from 5823 and 3988 patients from May 2021-February 2022 were entered in initial and follow-up forms on a REDCap database. The majority of patients who received counseling were satisfied. At follow-up, 98.4% of respondents reported that HHC prevented hospitalization, 76.5% reported they could manage their symptoms at home, and 69.5% reported that counseling helped to limit the spread of COVID-19 in their household. Conclusions: Telehealth can be an essential strategy for providing services while keeping patients and health providers safe during the COVID-19 pandemic.
MeSH term(s)	COVID-19/epidemiology ; Counseling ; Home Care Services ; Humans ; Nepal/epidemiology ; Pandemics
Language	English
Publishing date	2022-05-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2711781-9
ISSN	2296-2565 ; 2296-2565
ISSN (online)	2296-2565
ISSN	2296-2565
DOI	10.3389/fpubh.2022.891611
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Article ; Online: Loss of peri-Wolffian duct stromal Frs2α expression in mice leads to abnormal ureteric bud induction and vesicoureteral reflux.

Narla, Deepti / Slagle, Stacey B / Schaefer, Caitlin M / Bushnell, Daniel S / Puri, Pawan / Bates, Carlton M

Pediatric research

2017 Volume 82, Issue 6, Page(s) 1022–1029

Abstract: BackgroundFibroblast growth factor receptor 2 (Fgfr2) deletion from murine peri-Wolffian duct stroma (ST) results in aberrant ureteric bud induction, abnormal ureteral insertion into the bladder, and high rates of vesicoureteral reflux (VUR). It is ... ...

Abstract	BackgroundFibroblast growth factor receptor 2 (Fgfr2) deletion from murine peri-Wolffian duct stroma (ST) results in aberrant ureteric bud induction, abnormal ureteral insertion into the bladder, and high rates of vesicoureteral reflux (VUR). It is unclear which receptor docking protein(s) is/are responsible for Fgfr2 actions in these tissues. We investigated whether the docking protein, fibroblast receptor substrate 2α (Frs2α), had a role in peri-Wolffian duct ST similar to Fgfr2.MethodsWe conditionally deleted Frs2α in peri-Wolffian duct ST with a Tbx18cre mouse line (Frs2α Controls: Mutant refluxing ureters that inserted improperly into the bladder had shortened intravesicular tunnels (IVTs) when compared with controlsConclusionFrs2α
MeSH term(s)	Animals ; Apoptosis ; Bone Morphogenetic Protein 4/genetics ; Cell Proliferation ; Membrane Proteins/genetics ; Mice ; Mice, Knockout ; Ureter/embryology ; Ureter/pathology ; Vesico-Ureteral Reflux/genetics ; Wolffian Ducts/metabolism
Chemical Substances	Bmp4 protein, mouse ; Bone Morphogenetic Protein 4 ; FRS2alpha protein, mouse ; Membrane Proteins
Language	English
Publishing date	2017-08-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	4411-8
ISSN	1530-0447 ; 0031-3998
ISSN (online)	1530-0447
ISSN	0031-3998
DOI	10.1038/pr.2017.175
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