Purpose:The purpose of the study was to evaluate the presentation and management of posthysterectomy ureteral injuries.Patients and Methods:Fourteen patients with ureteric injuries after hysterectomy for benign diseases were evaluated. The diagnosis was done based on clinical presentation, intravenous urogram, computed tomography, cystoscopy, and retrograde pyelogram (RGP) depending on the clinical situation.Results:Sixteen iatrogenic ureteric injuries in 14 patients over a 2-year period were evaluated. Hysterectomy was the cause of injury in all the cases, 12 abdominal and 2 were vaginal. Two patients presented with anuria, one had ureteric, and bladder injury with hemoperitoneum underwent emergency laparotomy and bilateral ureteral reimplantation. Another patient underwent RGP followed by stenting on the right side, left side unable to put stent so percutaneous nephrostomy (PCN) was done followed by antegrade stenting later. Two patients presented with septicemia and pyonephrosis were managed initially with PCN followed by balloon dilatation and JJ stenting. RGP and retrograde stenting was done in seven of the remaining ten patients and ureteric reimplantation in three patients.Conclusion:Patient with ureteric injury should be evaluated and intervened at the earliest. Patients presenting early, within 2 weeks after hysterectomy have higher chances of success with endourological procedures, obviating the need for open surgery.
Aim:The study was aimed to assess the knowledge on understanding ethical authorship of research publications among the medical and pharmacy faculty members of India. Materials and Methods: We have selected 54 numbers of medical faculty members and 41 numbers of pharmacy faculty members from different parts of India to assess their understanding and knowledge on concept in authorship issues for ethical publication by questionnaire and telephone interview. Results: It showed a significant higher number of publications (t=3.765, p<0.001) including first authorship (t=15.34, p<0.001) among pharmacy faculty members as compared to medical faculty members. 74.07% of medical and 68.29% of pharmacy faculty members confessed that they did not have any discussion on authorship issues at anytime.88.88% of medical and 36.5% of pharmacy faculty members also mentioned that their Professors and Head of the departments were awarded 'gifted authorship'. 81.4% of medical and 29.26% of pharmacy faculty members also said that their seniors pressurized them to include their names in their manuscripts. Conclusions: Indicate a clear unethical practice on authorship issues among medical faculty members of India. Although pharmacy faculty members are better in practicing ethical authorship as compared to their medical counterparts but them too need lot of improvements on understanding ethical authorship.
Background:
Triple Negative Breast Cancer (TNBC) commonly displays Epidermal growth factor receptor (EGFR). Effective EGFR degradation results in suppression of tumor in various models. Studies have addressed the relevance of this strategy in the treatment of TNBC. In the present study, we examined the effect of 17 β-estradiol on EGFR expression in MDA-MB-231 (TNBC) cell line and assessed whether 17 β-estradiol degrades EGFR by ubiquitination pathway.
Objectives:
To treat MDA-MB-231 cell lines with Cycloheximide with or without 17β-estrdiol to observe whether 17β-estradiol leads to EGFR degradation. To treat with MG-132 to assess whether degradation occurs through ubiquitination pathway.
Methods:
MDA-MB-231 cells were treated with 17β-estradiol (E2) and EGFR expression was studied by western blotting at different intervals by using Cycloheximide chase. To assess the ubiquitination pathway of degradation of EGFR in MDA-MB-231 cell line, MG-132 was used.
Results:
EGFR expression was reduced with β-estradiol treatment in MDA-MB-231 cell line with Cycloheximide chase. Upon Treatment with MG-132 and E2, EGFR expression did not reduce, suggesting that Estrogen degrades EGFR by ubiquitination pathway.
Conclusion:
Estrogen degrades EGFR in MDA-MB-231 cells and this degradation occurs by ubiquitination.
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