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Article: Prophylactic administration of alpha-blockers for the prevention of post-operative urinary retention following inguinal hernia repair: A meta-analysis of randomized control trials.

Bhagat, Saumya / El-Kafsi, Jihene / Samraj, Kumarakrishnan / Mastoridis, Sotiris

The surgeon : journal of the Royal Colleges of Surgeons of Edinburgh and Ireland

2022 Volume 21, Issue 4, Page(s) e152–e158

Abstract: Background: Inguinal hernia repair is a commonly performed surgical procedure performed in adult males. Urinary retention following surgery is a known complication likely due to the adrenergic over-stimulation of smooth muscles in the bladder neck and ... ...

Abstract	Background: Inguinal hernia repair is a commonly performed surgical procedure performed in adult males. Urinary retention following surgery is a known complication likely due to the adrenergic over-stimulation of smooth muscles in the bladder neck and prostate. This effect could potentially be mitigated by the use of alpha-blocker medications. A meta-analysis of randomized control trials (RCTs) was performed to analyse the evidence behind the use of alpha-blockers in the prevention of post-operative urinary retention (POUR). Methods: A comprehensive search of PubMed, Embase, MedLine and Scopus was undertaken adhering to PRISMA guidelines. RCTs using alpha-blockers as a single point intervention were included. Data were analysed using a random-effects model. Risk of Bias (ROB) was assessed according to Cochrane guidelines. Results: Seven RCTs including 680 patients were included. The use of alpha-blockade reduced the incidence of urinary retention requiring catheterization (OR:0.23, 95% CI:0.07-0.70, p:0.009). No serious side-effects of alpha-blockers were reported. Conclusion: Alpha-blockers are a safe and effective intervention to reduce the incidence of urinary retention following inguinal hernia repair surgery.
MeSH term(s)	Adult ; Humans ; Male ; Adrenergic alpha-Antagonists/therapeutic use ; Hernia, Inguinal/surgery ; Hernia, Inguinal/etiology ; Herniorrhaphy/adverse effects ; Herniorrhaphy/methods ; Incidence ; Postoperative Complications/etiology ; Postoperative Complications/prevention & control ; Postoperative Complications/epidemiology ; Urinary Retention/etiology ; Urinary Retention/prevention & control ; Urinary Retention/epidemiology ; Randomized Controlled Trials as Topic
Chemical Substances	Adrenergic alpha-Antagonists
Language	English
Publishing date	2022-09-30
Publishing country	Scotland
Document type	Meta-Analysis ; Journal Article
ZDB-ID	2102927-1
ISSN	1479-666X
ISSN	1479-666X
DOI	10.1016/j.surge.2022.09.002
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Article ; Online: PGE

Khan, Gausal A / Bhagat, Saumya / Alam, Md Iqbal

Journal of leukocyte biology

2019 Volume 105, Issue 4, Page(s) 705–717

Abstract: ... ...

Abstract	PGE
MeSH term(s)	Brain/cytology ; Cell Movement/drug effects ; Chemotaxis/drug effects ; Cyclic AMP/biosynthesis ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Dinoprostone/pharmacology ; Endothelial Cells/cytology ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Extracellular Matrix/drug effects ; Extracellular Matrix/metabolism ; Humans ; Receptors, Prostaglandin E/metabolism
Chemical Substances	Receptors, Prostaglandin E ; Cyclic AMP (E0399OZS9N) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2019-03-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1002/JLB.2A0918-361R
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Zs.A 603: Show issues

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Article ; Online: Hypoxia induced up-regulation of tissue factor is mediated through extracellular RNA activated Toll-like receptor 3-activated protein 1 signalling.

Bhagat, Saumya / Biswas, Indranil / Ahmed, Rehan / Khan, Gausal A

Blood cells, molecules & diseases

2020 Volume 84, Page(s) 102459

Abstract: Sterile Inflammation (SI), a condition where damage associated molecular patterns (DAMPs) released from dying cells, leads to TLR (Toll-like receptor) activation and triggers hypoxemia in circulation leading to venous thrombosis (VT) through tissue ... ...

Abstract	Sterile Inflammation (SI), a condition where damage associated molecular patterns (DAMPs) released from dying cells, leads to TLR (Toll-like receptor) activation and triggers hypoxemia in circulation leading to venous thrombosis (VT) through tissue factor (TF) activation, but its importance under acute hypoxia (AH) remains unexplored. Thus, we hypothesized that eRNA released from dying cells under AH activates TF via the TLR3-ERK1/2-AP1 pathway, leading to VT. Animals were exposed to stimulate hypoxia for 0-24 h at standard temperature and humidity. RNaseA and DNase1 were injected immediately before exposure. TLR3 gene silencing was performed through in vivo injection of TLR3 siRNA. 80 μg/kg BW of isolated eRNA and eDNA were injected 6 h prior to sacrifice. Antigens of TF pathway were determined by ELISA and TF activity by a chromogenic assay. AH exposure significantly induced release of SI markers i.e. eRNA, eDNA, HMGB1 and upregulated TLR3, ERK1/2 (Extracellular signal-regulated kinases), AP1 (Activator Protein-1) and TF, whereas RNaseA pre-treatment diminished the effect of AH, thus inhibiting TF expression as well as activity during AH. Hence, we propose a possible mechanism of AH-induced TF activation and thrombosis where RNaseA can become the novel focal point in ameliorating therapy for AH induced thrombosis.
MeSH term(s)	Animals ; Cells, Cultured ; Hypoxia/complications ; Hypoxia/genetics ; Hypoxia/metabolism ; MAP Kinase Signaling System ; Mice ; RNA/metabolism ; Replication Protein C/metabolism ; Signal Transduction ; Thromboplastin/genetics ; Thromboplastin/metabolism ; Thrombosis/etiology ; Thrombosis/genetics ; Thrombosis/metabolism ; Toll-Like Receptor 3/metabolism ; Up-Regulation
Chemical Substances	TLR3 protein, mouse ; Toll-Like Receptor 3 ; RNA (63231-63-0) ; Thromboplastin (9035-58-9) ; Replication Protein C (EC 3.6.4.-)
Keywords	covid19
Language	English
Publishing date	2020-06-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1237083-6
ISSN	1096-0961 ; 1079-9796
ISSN (online)	1096-0961
ISSN	1079-9796
DOI	10.1016/j.bcmd.2020.102459
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Article ; Online: Key role of Extracellular RNA in hypoxic stress induced myocardial injury.

Bhagat, Saumya / Biswas, Indranil / Alam, Md Iqbal / Khan, Madiha / Khan, Gausal A

PloS one

2021 Volume 16, Issue 12, Page(s) e0260835

Abstract: Myocardial infarction (MI), atherosclerosis and other inflammatory and ischemic cardiovascular diseases (CVDs) have a very high mortality rate and limited therapeutic options. Although the diagnosis is based on markers such as cardiac Troponin-T (cTrop-T) ...

Abstract	Myocardial infarction (MI), atherosclerosis and other inflammatory and ischemic cardiovascular diseases (CVDs) have a very high mortality rate and limited therapeutic options. Although the diagnosis is based on markers such as cardiac Troponin-T (cTrop-T), the mechanism of cTrop-T upregulation and release is relatively obscure. In the present study, we have investigated the mechanism of cTrop-T release during acute hypoxia (AH) in a mice model by ELISA & immunohistochemistry. Our study showed that AH exposure significantly induces the expression and release of sterile inflammatory as well as MI markers in a time-dependent manner. We further demonstrated that activation of TLR3 (mediated by eRNA) by AH exposure in mice induced cTrop-T release and Poly I:C (TLR3 agonist) also induced cTrop-T release, but the pre-treatment of TLR3 immuno-neutralizing antibody or silencing of Tlr3 gene or RNaseA treatment two hrs before AH exposure, significantly abrogated AH-induced Caspase 3 activity as well as cTrop-T release. Our immunohistochemistry and Masson Trichrome (MT) staining studies further established the progression of myocardial injury by collagen accumulation, endothelial cell and leukocyte activation and adhesion in myocardial tissue which was abrogated significantly by pre-treatment of RNaseA 2 hrs before AH exposure. These data indicate that AH induced cTrop-T release is mediated via the eRNA-TLR3-Caspase 3 pathway.
MeSH term(s)	Animals ; Apoptosis ; Caspase 3/genetics ; Caspase 3/metabolism ; Disease Models, Animal ; Extracellular Vesicles/genetics ; Hypoxia/physiopathology ; Mice ; Myocardial Infarction/genetics ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; RNA/genetics ; RNA/metabolism ; Signal Transduction ; Toll-Like Receptor 3/genetics ; Toll-Like Receptor 3/metabolism ; Troponin T/metabolism
Chemical Substances	TLR3 protein, mouse ; TNNT2 protein, human ; Toll-Like Receptor 3 ; Troponin T ; RNA (63231-63-0) ; CASP3 protein, human (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-)
Language	English
Publishing date	2021-12-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0260835
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Article ; Online: Key role of Extracellular RNA in hypoxic stress induced myocardial injury.

Saumya Bhagat / Indranil Biswas / Md Iqbal Alam / Madiha Khan / Gausal A Khan

PLoS ONE, Vol 16, Iss 12, p e

2021 Volume 0260835

Abstract	Myocardial infarction (MI), atherosclerosis and other inflammatory and ischemic cardiovascular diseases (CVDs) have a very high mortality rate and limited therapeutic options. Although the diagnosis is based on markers such as cardiac Troponin-T (cTrop-T), the mechanism of cTrop-T upregulation and release is relatively obscure. In the present study, we have investigated the mechanism of cTrop-T release during acute hypoxia (AH) in a mice model by ELISA & immunohistochemistry. Our study showed that AH exposure significantly induces the expression and release of sterile inflammatory as well as MI markers in a time-dependent manner. We further demonstrated that activation of TLR3 (mediated by eRNA) by AH exposure in mice induced cTrop-T release and Poly I:C (TLR3 agonist) also induced cTrop-T release, but the pre-treatment of TLR3 immuno-neutralizing antibody or silencing of Tlr3 gene or RNaseA treatment two hrs before AH exposure, significantly abrogated AH-induced Caspase 3 activity as well as cTrop-T release. Our immunohistochemistry and Masson Trichrome (MT) staining studies further established the progression of myocardial injury by collagen accumulation, endothelial cell and leukocyte activation and adhesion in myocardial tissue which was abrogated significantly by pre-treatment of RNaseA 2 hrs before AH exposure. These data indicate that AH induced cTrop-T release is mediated via the eRNA-TLR3-Caspase 3 pathway.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Key role of Extracellular RNA in hypoxic stress induced myocardial injury

Saumya Bhagat / Indranil Biswas / Md Iqbal Alam / Madiha Khan / Gausal A. Khan

PLoS ONE, Vol 16, Iss

2021 Volume 12

Abstract	Myocardial infarction (MI), atherosclerosis and other inflammatory and ischemic cardiovascular diseases (CVDs) have a very high mortality rate and limited therapeutic options. Although the diagnosis is based on markers such as cardiac Troponin-T (cTrop-T), the mechanism of cTrop-T upregulation and release is relatively obscure. In the present study, we have investigated the mechanism of cTrop-T release during acute hypoxia (AH) in a mice model by ELISA & immunohistochemistry. Our study showed that AH exposure significantly induces the expression and release of sterile inflammatory as well as MI markers in a time-dependent manner. We further demonstrated that activation of TLR3 (mediated by eRNA) by AH exposure in mice induced cTrop-T release and Poly I:C (TLR3 agonist) also induced cTrop-T release, but the pre-treatment of TLR3 immuno-neutralizing antibody or silencing of Tlr3 gene or RNaseA treatment two hrs before AH exposure, significantly abrogated AH-induced Caspase 3 activity as well as cTrop-T release. Our immunohistochemistry and Masson Trichrome (MT) staining studies further established the progression of myocardial injury by collagen accumulation, endothelial cell and leukocyte activation and adhesion in myocardial tissue which was abrogated significantly by pre-treatment of RNaseA 2 hrs before AH exposure. These data indicate that AH induced cTrop-T release is mediated via the eRNA-TLR3-Caspase 3 pathway.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Hypoxia induced up-regulation of tissue factor is mediated through extracellular RNA activated Toll-like receptor 3-activated protein 1 signalling

Bhagat, Saumya / Biswas, Indranil / Ahmed, Rehan / Khan, Gausal A.

Blood Cells Mol Dis

Abstract	Sterile Inflammation (SI), a condition where damage associated molecular patterns (DAMPs) released from dying cells, leads to TLR (Toll-like receptor) activation and triggers hypoxemia in circulation leading to venous thrombosis (VT) through tissue factor (TF) activation, but its importance under acute hypoxia (AH) remains unexplored. Thus, we hypothesized that eRNA released from dying cells under AH activates TF via the TLR3-ERK1/2-AP1 pathway, leading to VT. Animals were exposed to stimulate hypoxia for 0–24 h at standard temperature and humidity. RNaseA and DNase1 were injected immediately before exposure. TLR3 gene silencing was performed through in vivo injection of TLR3 siRNA. 80 μg/kg BW of isolated eRNA and eDNA were injected 6 h prior to sacrifice. Antigens of TF pathway were determined by ELISA and TF activity by a chromogenic assay. AH exposure significantly induced release of SI markers i.e. eRNA, eDNA, HMGB1 and upregulated TLR3, ERK1/2 (Extracellular signal-regulated kinases), AP1 (Activator Protein-1) and TF, whereas RNaseA pre-treatment diminished the effect of AH, thus inhibiting TF expression as well as activity during AH. Hence, we propose a possible mechanism of AH-induced TF activation and thrombosis where RNaseA can become the novel focal point in ameliorating therapy for AH induced thrombosis.
Keywords	covid19
Publisher	Elsevier; PMC
Document type	Article ; Online
DOI	10.1016/j.bcmd.2020.102459
Database	COVID19

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Article ; Online: Protective effects of novel diazepinone derivatives in snake venom induced sterile inflammation in experimental animals.

Alam, M I / Quasimi, Huma / Kumar, Amit / Alam, Aftab / Bhagat, Saumya / Alam, M Sarwar / Khan, G A / Dhulap, Abhijeet / Ahmad Ansari, Mairaj

European journal of pharmacology

2022 Volume 928, Page(s) 175095

Abstract: Snake envenomation leads to the formation of damage-associated molecular patterns (DAMPs), which are mediated by endogenous intracellular molecules. These are recognized by pattern-recognition receptors (PRRs) and can induce sterile inflammation.: Aims! ...

Abstract	Snake envenomation leads to the formation of damage-associated molecular patterns (DAMPs), which are mediated by endogenous intracellular molecules. These are recognized by pattern-recognition receptors (PRRs) and can induce sterile inflammation. Aims: In the present study, we aim at understanding the mechanisms involved in DAMPs induced sterile inflammation to unravel the novel therapeutic strategies for treating snake bites. The potential of benzodiazepinone derivatives to act against snake venom induced inflammation has been explored in the present investigation. Main methods: Three compounds VA 17, VA 43 and PA 03 were taken from our library of synthetic compounds. Oxidative stress markers such as lipid peroxidation, superoxide and nitric oxide were measured along with the analysis of DAMPs (IL6, HMGB1, vWF, S100b and HSP70). These compounds have been docked using molecular docking against the snake venom PLA Key findings: The compounds have been found to effectively neutralize viper and cobra venoms induced lethal activity both ex vivo and in vivo. The compounds have also neutralized the viper venom induced hemorrhagic, coagulant, anticoagulant reactions as well as inflammation. The fold of protection have always been found to be higher in case of ex vivo than in in vivo. These compounds have neutralized the venom induced DAMPs as exhibited by IL6, HMGB1, vWF, S100b and HSP70. The fold of neutralization is found to be higher in VA 43. Significance: The identified compounds could be used as potential candidates for developing treatment of snakebites in areas where antiserums are not yet available.
MeSH term(s)	Animals ; Antivenins/chemistry ; Antivenins/pharmacology ; Antivenins/therapeutic use ; HMGB1 Protein ; Inflammation/chemically induced ; Inflammation/drug therapy ; Interleukin-6 ; Molecular Docking Simulation ; Snake Bites/drug therapy ; Viper Venoms ; von Willebrand Factor
Chemical Substances	Antivenins ; HMGB1 Protein ; Interleukin-6 ; Viper Venoms ; von Willebrand Factor
Language	English
Publishing date	2022-06-18
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2022.175095
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Zs.A 522: Show issues

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Article ; Online: Sterile Inflammatory Role of High Mobility Group Box 1 Protein: Biological Functions and Involvement in Disease.

Gonelevue, Sera / Bandyopadhyay, Abhirup / Bhagat, Saumya / Alam, Md Iqbal / Khan, Gausal A

Journal of vascular research

2018 Volume 55, Issue 4, Page(s) 244–254

Abstract: High mobility group box 1 protein (HMGB1), a sterile inflammatory molecule and damage-associated molecular pattern (DAMP) released from various cells during stress has been implicated in inflammation. Several reports show that there is a direct ... ...

Abstract	High mobility group box 1 protein (HMGB1), a sterile inflammatory molecule and damage-associated molecular pattern (DAMP) released from various cells during stress has been implicated in inflammation. Several reports show that there is a direct relationship between inflammation and cardiovascular diseases (CVDs) such as thrombosis, hypertension, insulin resistance, preeclampsia, etc. Here, we intend to summarize the concept of the emerging link between HMGB1 and CVDs. Furthermore, we will discuss the possible therapeutic strategies that target HMGB1 for the treatment of different CVDs.
MeSH term(s)	Animals ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/physiopathology ; Coronary Disease/physiopathology ; Disseminated Intravascular Coagulation/physiopathology ; Female ; HMGB1 Protein/antagonists & inhibitors ; HMGB1 Protein/physiology ; Humans ; Inflammation/physiopathology ; Oxidation-Reduction ; Pre-Eclampsia/physiopathology ; Pregnancy ; Signal Transduction ; Stroke/physiopathology ; Venous Thrombosis/physiopathology
Chemical Substances	HMGB1 Protein
Language	English
Publishing date	2018-09-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1105259-4
ISSN	1423-0135 ; 1018-1172
ISSN (online)	1423-0135
ISSN	1018-1172
DOI	10.1159/000491390
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Article ; Online: Inhibition of snake venom induced sterile inflammation and PLA2 activity by Titanium dioxide Nanoparticles in experimental animals.

Chakrabartty, Shubhro / Alam, Md Iqbal / Bhagat, Saumya / Alam, Aftab / Dhyani, Neha / Khan, Gausal A / Alam, M Sarwar

Scientific reports

2019 Volume 9, Issue 1, Page(s) 11175

Abstract: Sterile inflammation (SI) is an essential process in response to snakebite and injury. The venom induced pathophysiological response to sterile inflammation results into many harmful and deleterious effects that ultimately leads to death. The available ... ...

Abstract	Sterile inflammation (SI) is an essential process in response to snakebite and injury. The venom induced pathophysiological response to sterile inflammation results into many harmful and deleterious effects that ultimately leads to death. The available treatment for snakebite is antiserum which does not provide enough protection against venom-induced pathophysiological changes like haemorrhage, necrosis, nephrotoxicity and often develop hypersensitive reactions. In order to overcome these hindrances, scientists around the globe are searching for an alternative therapy to provide better treatment to the snake envenomation patients. In the present study TiO
MeSH term(s)	Animals ; Animals, Laboratory ; Elapid Venoms ; Hemorrhage/prevention & control ; Inflammation/prevention & control ; Mice ; Nanoparticles/chemistry ; Nanoparticles/therapeutic use ; Necrosis/prevention & control ; Phospholipases A2/metabolism ; Snake Bites/pathology ; Snake Bites/physiopathology ; Snake Bites/therapy ; Snake Venoms/antagonists & inhibitors ; Snake Venoms/toxicity ; Titanium/therapeutic use ; Viper Venoms
Chemical Substances	Elapid Venoms ; Naja kaouthia venom ; Snake Venoms ; Viper Venoms ; titanium dioxide (15FIX9V2JP) ; Titanium (D1JT611TNE) ; Phospholipases A2 (EC 3.1.1.4)
Language	English
Publishing date	2019-08-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-47557-y
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