Jugaad Trocar for a 5-mm Laparoscopic Cannula

xlomafota.13 shared this article with you from Inoreader Jugaad Trocar for a 5-mm Laparoscopic Cannula Via Latest Results for Indian Journal of Surgery Abstract When we are practicing, especially in rural India, we often face problems of instrument failure or lost instrument, etc... which may sometimes necessitate abandoning the procedure just because of the lack of a single instrument. We do mobile laparoscopic surgery, carrying all the laparoscopic instruments to far-off places, as far as 60–80 km. On one such occasion, my staff had lost a 5-mm trocar, which had gone unnoticed until I posted a case for laparoscopic cholecystectomy. There was not much time to buy a new one and also it was difficult to procure from the dealer because of the COVID-19 situation. Just because of the lack of one instrument we were facing a situation of postponing laparoscopy! View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Adjusting to ostomy: The Good, the Bad and the Ugly side of post ostomy Life issues in a cohort of Indian patients

xlomafota.13 shared this article with you from Inoreader Adjusting to ostomy: The Good, the Bad and the Ugly side of post ostomy Life issues in a cohort of Indian patients Via Latest Results for Indian Journal of Surgery Abstract Problems faced by patients in adapting to life after stoma surgery can be affected by a multitude of factors including socioeconomic and clinical parameters. In India, a huge number of stoma surgeries are performed everyday with limited facility of specialised stoma care. Hence, this study seeks to explore and proportionally weigh the challenges faced by these patients in various aspects in order to channelise the information gained towards improved outcome. The study was conducted on 69 patients at the Department of Surgery in a tertiary care setting in eastern India. The instrument used was a three-section Questionnaire which included City of Hope National Medical Centre Questionnaire on Quality of Life, Acceptance of Illness Scale and Ostomy Adjustment Inventory 23. Mean total quality of life score 148.24 with lowest scores in the social domain. Average acceptance of illness score is 1.97 ± 0.11. Average adjustment score is 2.99. Factors like gender and the t ype of stoma (permanent or temporary) affected the quality of life and acceptance of illness outcomes. Age influenced psychosocial adjustment. Gender and type of stoma, i.e. temporary or permanent, have an impact on the perceived quality of life and acceptance level. Age influences level of adjustment to ostomy. This study revealed the specific issues which posed the biggest difficulties in adapting to a stoma in physical psychological as well as social domains among Indian patients. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Dr. Edward E. Mason: Father of Bariatric Surgery

xlomafota.13 shared this article with you from Inoreader Dr. Edward E. Mason: Father of Bariatric Surgery Via Latest Results for Indian Journal of Surgery Abstract Dr. Edward E. Mason rightly called the "father of bariatric surgery" has roots deep in Iowa where he spent most of his professional and academic life. Edward E Mason was the first to perform gastric bypass surgeries for weight reduction. Later, Mason and his associates started performing vertical banded gastroplasties. Dr. Edward E. Mason was also instrumental in establishing the American Society of Bariatric Surgery. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

The Roux-en-Y Lateral Duodenojejunostomy: an Elegant Solution for Traumatic Pediatric Duodenal Disruption

xlomafota.13 shared this article with you from Inoreader The Roux-en-Y Lateral Duodenojejunostomy: an Elegant Solution for Traumatic Pediatric Duodenal Disruption Via Latest Results for Indian Journal of Surgery Abstract Duodenal trauma is rare in children and its diagnosis and management often pose a challenge. In complex duodenal injuries, primary closure may not be feasible and complications are prone to occur in the post-operative period. Herein, we share our experience of such a case managed by an infrequently utilized technique, Roux-en-Y lateral duodenojejunostomy. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Inflammation Triggered by SARS-CoV-2 and ACE2 Augment Drives Multiple Organ Failure of Severe COVID-19: Molecular Mechanisms and Implications

xlomafota.13 shared this article with you from Inoreader Inflammation Triggered by SARS-CoV-2 and ACE2 Augment Drives Multiple Organ Failure of Severe COVID-19: Molecular Mechanisms and Implications Via Latest Results Abstract The widespread occurrence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to a pandemic of coronavirus disease 2019 (COVID-19). The S spike protein of SARS-CoV-2 binds with angiotensin-converting enzyme 2 (ACE2) as a functional "receptor" and then enters into host cells to replicate and damage host cells and organs. ACE2 plays a pivotal role in the inflammation, and its downregulation may aggravate COVID-19 via the renin-angiotensin system, including by promoting pathological changes in lung injury and involving inflammatory responses. Severe patients of COVID-19 often develop acute respiratory distress syndrome and multiple organ dysfunction/failure with high mortality that may be closely related to the hyper-proinflammatory status called the "cytokine storm." Massive cytokines including interleukin-6, nuclear factor kappa B (NFκB), and tumor necrosis factor alpha (TNFα) released from SARS-CoV-2-infected macrophages a nd monocytes lead inflammation-derived injurious cascades causing multi-organ injury/failure. This review summarizes the current evidence and understanding of the underlying mechanisms of SARS-CoV-2, ACE2 and inflammation co-mediated multi-organ injury or failure in COVID-19 patients. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

The Protective Effects of Perindopril Against Acute Kidney Damage Caused by Septic Shock

xlomafota.13 shared this article with you from Inoreader The Protective Effects of Perindopril Against Acute Kidney Damage Caused by Septic Shock Via Latest Results Abstract Acute kidney injury (AKI) resulting from septic shock caused by sepsis is an important health problem encountered at rates of 55–73%. Increasing oxidative stress and inflammation following sepsis is a widely observed condition with rising mortality rates. The purpose of this study was to determine whether perindopril (PER) can prevent sepsis-associated AKI with its antioxidant, anti-inflammatory, and anti-apoptotic effects. The control group received an oral saline solution only for 4 days. Cecal ligation and puncture (CLP)–induced sepsis only was applied to the CLP group, while the CLP + PER (2 mg/kg) received CLP-induced sepsis together with 2 mg/kg PER via the oral route for 4 days before induction of sepsis. Finally, all rats were euthanized by anesthesia and sacrificed. TBARS, total SH levels and NF-κβ, TNF-α, and Caspase-3 expression were then calculated for statistical analysis. TBARS, total SH, NF-kβ/p65, TNF-a, and Caspase-3 levels increased in the CLP group. In contrast, oral administration of PER (2 mg/kg) to septic rats reduced TBARS levels and NF-kβ/p65, TNF-α, and Caspase-3 immunopositivity at biochemical analysis. PER treatment appears to be a promising method for preventing sepsis-induced acute kidney injury through its antioxidant anti-inflammation and anti-apoptotic activities. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

LncRNA MEG3 Participates in Caerulein-Induced Inflammatory Injury in Human Pancreatic Cells via Regulating miR-195-5p/FGFR2 Axis and Inactivating NF-κB Pathway

xlomafota.13 shared this article with you from Inoreader LncRNA MEG3 Participates in Caerulein-Induced Inflammatory Injury in Human Pancreatic Cells via Regulating miR-195-5p/FGFR2 Axis and Inactivating NF-κB Pathway Via Latest Results Abstract Acute pancreatitis (AP) is a dysfunctional pancreas disease marked by severe inflammation. Long non-coding RNAs (lncRNAs) involving in the regulation of inflammatory responses have been frequently mentioned. The purpose of this study was to ensure the function and action mode of lncRNA maternally expressed gene 3 (MEG3) in caerulein-induced AP cell model. HPDE cells were treated with caerulein to establish an AP model in vitro. The expression of MEG3, miR-195-5p, and fibroblast growth factor receptor 2 (FGFR2) was measured using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation and apoptosis were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry assay, respectively. The expression of CyclinD1, B cell lymphoma/leukemia-2 (Bcl-2), Bcl-2-associated X protein (Bax), FGFR2, P65, phosphorylated P65 (p-P65), alpha inhibitor of nuclear factor kappa beta (NF-κB) (IκB-α), and phosphorylated IκB-α (p-IκB-α) at the protein level was quantified by western blot. The concentrations of tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) were monitored by enzyme-linked immunosorbent assay (ELISA). The targeted relationship between miR-195-5p and MEG3 or FGFR2 was forecasted by the online software starBase v2.0 and verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. As a result, the expression of MEG3 and FGFR2 was decreased in caerulein-induced HPDE cells, while the expression of miR-195-5p was increased. MEG3 overexpression inhibited cell apoptosis and inflammatory responses that were induced by caerulein. Mechanically, miR-195-5p was targeted by MEG3 and abolished the effects of MEG3 overexpression. FGFR2 was a target of miR-195-5p, and MEG3 regulated the expression of FGFR2 by sponging miR-195-5p. FGFR2 overexpression abolished miR-195-5p enrichment-aggravated inflammatory injuries. M oreover, the NF-κB signaling pathway was involved in the MEG3/miR-195-5p/FGFR2 axis. Collectively, MEG3 participates in caerulein-induced inflammatory injuries by targeting the miR-195-5p/FGFR2 regulatory axis via mediating the NF-κB pathway in HPDE cells. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Effect of Exclusive Enteral Nutrition on Th17 Cells in Juvenile Rats with Inflammatory Bowel Disease

xlomafota.13 shared this article with you from Inoreader Effect of Exclusive Enteral Nutrition on Th17 Cells in Juvenile Rats with Inflammatory Bowel Disease Via Latest Results Abstract The objective was to investigate the effect of exclusive enteral nutrition (EEN) on T helper (Th) 17 cells by observing the effects of EEN on colon and serum interleukin (IL)-17A levels in juvenile inflammatory bowel disease (IBD) rat models and to reveal the potential mechanism of the therapeutic effect of EEN on IBD. ATNBS-induced IBD rat model was established. Feeding Peptison, a type of enteric nutrition (EN) for EEN-IBD group and EEN group, normal feed for IBD model group and control group for six consecutive days. Four groups of juvenile rats were sacrificed on day 7. The pathology of the intestinal mucosa was examined, the expression of IL-17A in serum was detected by ELISA, and the expression of IL-17A in intestinal tissue was detected by both western blot and real-time PCR (RT-PCR). Diarrhea, bloody stools, and weight loss were found in both the IBD group and the EEN-IBD group. After 5 days of EEN feeding, the stool characteristics, and blood in the st ools of the rats in the EEN-IBD group were significantly relieved compared with those of the IBD group. There was no significant difference in the body mass growth rate between the IBD group and EEN-IBD group (P > 0.05). The growth rate of the EEN group was 51.29 ± 3.61%, which was significantly lower than that of the control group (60.17 ± 9.32%) with P < 0.05. The disease activity index (DAI) score of the EEN-IBD group was significantly lower than that of the IBD group (P < 0.05). In the IBD group, colonic congestion and edema were obvious, scattered ulcers were observed, and the intestinal mucosa had a large amount of inflammatory cell infiltration. In the EEN-IBD group, the intestinal mucosa was slightly congested and a small amount of inflammatory cell infiltrated. The serum IL-17A expression level in the IBD group was significantly higher than in the EEN-IBD group, control group, and EEN group (P < 0.05). Both the gene and prot ein expressions of IL-17A in the intestinal tissue of the EEN-IBD group were significantly lower than in the IBD group (P < 0.01), and it was significantly higher in the IBD group than in the control and EEN groups (P < 0.01). EEN effectively reduced the intestinal inflammation in the juvenile rats with IBD. The mechanism could be related to the regulation of Th17 cells and the expression of the corresponding cytokine, IL-17A. EEN may play a role in downregulating the expression of IL-17A in the intestinal mucosa. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Electroacupuncture Reduces Inflammation but Not Bone Loss on Periodontitis in Arthritic Rats

xlomafota.13 shared this article with you from Inoreader Electroacupuncture Reduces Inflammation but Not Bone Loss on Periodontitis in Arthritic Rats Via Latest Results Abstract Periodontitis and rheumatoid arthritis (RA) are inflammatory diseases characterized by chronic inflammation and bone erosion. Electroacupuncture (EA) shows anti-inflammatory and anti-resorptive effects in experimental periodontitis (EP) and in RA. It is important to investigate whether EA shows these effects in periodontal tissues in the presence of these two inflammatory diseases or not. For this, Wistar rats were divided into six groups: control (C); experimental rheumatoid arthritis (RA; bovine type II collagen-induced (CII)); experimental periodontitis (EP); RA/EP (RA + EP); EP/EA (EP treated with EA); RA/EP/EA (RA + EP treated with EA). EP was induced 21 days after RA induction and EA was performed previously and during the EP induction period, every 3 days until the 36th experimental day. The rats were euthanized on day 39. RA was evaluated by edema and the withdrawal threshold of hind paws. The maxillae were removed, and alveolar bone loss (ABL ) and bone radiographic density (BRD) were evaluated. Immunohistochemical analyses for interleukins (IL)-6 and -17 and nuclear factor (NF)-κB were performed. Our results showed that EA reduced only the pain intensity in arthritic rats. Histomorphometric, macroscopic, and radiographic analyses did not show differences between the control and EP/EA groups. EA caused a reduction in ABL and BRD only in the presence of EP. EA caused a reduction in IL-6 and -17 in all groups, but NF-κB was only reduced in the arthritic rats with EP. In conclusion, EA reduced the inflammation related to periodontitis in arthritic rats but did not prevent ABL. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

GLP-1R Agonist Liraglutide Attenuates Inflammatory Reaction and Neuronal Apoptosis and Reduces Early Brain Injury After Subarachnoid Hemorrhage in Rats

xlomafota.13 shared this article with you from Inoreader GLP-1R Agonist Liraglutide Attenuates Inflammatory Reaction and Neuronal Apoptosis and Reduces Early Brain Injury After Subarachnoid Hemorrhage in Rats Via Latest Results Abstract Liraglutide, one of the glucagon-like peptide 1 receptor (GLP-1R) agonists, has been demonstrated to protect brain damage produced by ischemic stroke. However, it remains unknown whether liraglutide attenuates early brain injury after subarachnoid hemorrhage. The present study was performed to explore the effect of liraglutide on early brain injury after subarachnoid hemorrhage in rats, and further investigate the potential mechanisms. Sprague-Dawley rats underwent subarachnoid hemorrhage (SAH) by endovascular perforation, then received subcutaneous injection with liraglutide (50 or 100 μg/kg) or vehicle after 2 and 12 h of SAH. SAH grading, neurological scores, brain water content, and Evans Blue extravasation were measured 24 h after SAH. Immunofluorescent staining was performed to detect the extent of microglial activation in rat brain 24 h after SAH. TUNEL staining was performed to evaluate neuronal apoptosis in rat brain of SAH. Expression of GLP-1R, cycl ooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), Bcl-2, Bax, and cleaved caspase-3 in rat brain were determined by western blot. Expression of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in rat brain was assessed by ELISA. Neurological dysfunction, brain water content, Evans Blue extravasation, microglial activation, and neuronal apoptosis were significantly reduced by GLP-1R agonist liraglutide. Expression of GLP-1R in rat brain was decreased after SAH, which is significantly elevated by liraglutide. Expression of inflammatory mediates like COX-2, iNOS, TNF-α, and IL-1β was increased after SAH, which were significantly inhibited by liraglutide. Furthermore, SAH caused the elevated expression of pro-apoptotic factors Bax and cleaved caspase-3 in rat brain, both of which were inhibited by liraglutide. In addition, liraglutide reversed the expression of anti-apoptotic protein Bcl-2. Our results demonstrated that liraglutide reduces early brain injury and attenuates inflammatory reaction and neuronal apoptosis in rats of SAH. Liraglutide provides neuroprotection against SAH, which might be associated with the inhibition of inflammation and apoptosis. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Interleukin-1β Protection Against Experimental Sepsis

xlomafota.13 shared this article with you from Inoreader Interleukin-1β Protection Against Experimental Sepsis in Mice Via Latest Results Abstract The inflammatory response involving interleukin-1β (IL-1β) has been thought to play an important role in the development of late-phase sepsis. However, in this study, we wanted to explore the possibility of using IL-1β to improve the prognosis of sepsis by triggering local differentiation of bone marrow cells (BMCs) into regulatory dendritic cells (DCs) in vivo, thereby reversing the immune paralysis in late-phase sepsis. Sepsis mouse models were induced by cecal ligation and puncture (CLP) and lethal Escherichia coli O18 infection. Mice were injected intraperitoneally with IL-1β after CLP and after the lethal infection. Septic BMCs and liver immune cells were isolated at 0, 3, 6, 9, and 14 days post-CLP. BMCs and liver cells isolated from septic mice treated with IL-1β were adoptively transferred into CLP mice. GFP+-C57BL/6 parabiosis models were established. Serum IL-1β levels were determined by enzyme-linked immunosorbent a ssay (ELISA) kit, and the number, ratio, and phenotype of immune cells were observed by flow cytometry. IL-1β treatment improved the survival of sepsis and increased the numbers of BMCs and liver immune cells in septic mice. Moreover, IL-1β stimulation increased the number and the percentage of CD11c−CD45RBhigh DCs in septic BM and liver. Adoptive transfer of septic BMCs, liver immune cells, and CD11c−CD45RBhigh DCs treated with IL-1β into CLP mice attenuated sepsis. IL-1β triggered the redistribution of CD11c−CD45RBhigh DCs as well as BMCs in parabiosis models. IL-1β protects against sepsis by stimulating local proliferation and differentiation of BMCs into CD11c−CD45RBhigh DCs at immune organs and non-immune organs. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

S100A9 Upregulation Contributes to Learning and Memory Impairments by Promoting Microglia M1 Polarization in Sepsis Survivor Mice

xlomafota.13 shared this article with you from Inoreader S100A9 Upregulation Contributes to Learning and Memory Impairments by Promoting Microglia M1 Polarization in Sepsis Survivor Mice Via Latest Results Abstract Sepsis-associated encephalopathy (SAE) is a clinical syndrome of brain dysfunction secondary to sepsis, which is characterized by long-term neurocognitive deficits such as memory, attention, and executive dysfunction. However, the mechanisms underlying SAE remain unclear. By using transcriptome sequencing approach, we showed that hippocampal S100A9 was significantly increased in sepsis induced by cecal ligation and puncture (CLP) or lipopolysaccharide (LPS) challenge. Thus, we used S100A9 inhibitor Paquinimod to study the role of S100A9 in cognitive impairments in CLP-induced and LPS-induced mice models of SAE. Sepsis survivor mice underwent behavioral tests or the hippocampal tissues subjected to Western blotting, real-time quantitative PCR, and immunohistochemistry. Our results showed that CLP-induced and LPS-induced memory impairments were accompanied with increased expressions of hippocampal microglia Iba1 and CD86 (M1 markers), but reduced expression of Ar g1 (M2 marker). Notably, S100A9 inhibition significantly improved the survival rate and learning and memory impairments in sepsis survivors, with a shift from M1 to M2 phenotype. Taken together, our study suggests that S100A9 upregulation might contribute to learning and memory impairments by promoting microglia M1 polarization in sepsis survivors, whereas S100A9 inhibition might provide a potential therapeutic target for SAE. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.