A new and easy technique of double-J stenting after retroperitoneal laparoscopic ureterolithotomy: A discussion of other techniques.

AIM: To summarize a new and easy technique of double-J stent (DJ stent) placement after retroperitoneal laparoscopic ureterolithotomy (RLU). MATERIALS AND METHODS: RLU for upper and upper half of mid ureteric stones was performed successfully in 172 patients during the 8-year period between March 2011 and February 2019. In all the cases, a ureteric DJ stent was successfully placed by this new technique. A small-bore antral puncture needle is inserted into the retroperitoneal space to push down a DJ stent with a guidewire into the lower ureter. The tip of the antral puncture needle is manipulated to bring it near the ureterotomy site for easy insertion of the stent. The whole stent is pushed down leaving only the upper end in the ureterotomy area. Then, the guidewire is removed and the upper end is pushed up slowly into the renal pelvis. RESULTS: DJ stents were successfully inserted by this technique in all the 172 cases. In most cases, the stent could be placed in <3 min (range between 2 and 8 min). In two patients, the upper end failed to fully coil in the renal pelvis, but as the stent was passed beyond the ureterotomy site, it served its purpose of an internal drain. None of our cases had any urinary leak. Stents were removed cystoscopically after 6-12 weeks. CONCLUSION: This technique provides an easy, fast, and safe antegrade method of inserting a DJ stent after RLU.

Precocious anaphase and expression of Securin and p53 genes as candidate biomarkers for the early detection in areca nut-induced carcinogenesis.

Research over the years has generated enough evidence to implicate areca nut, as a carcinogen in humans. Besides oral, significant rise in the incidence of cancers of the oesophagus, liver and stomach was seen among areca nut chewers. Early diagnosis seems key to understand the initial processes of carcinogenesis which is highly curable. In North-East India, betel quid contains raw areca nut (RAN), lime and small portion of betel leaf without any other constituents. This study was not intended to isolate any active ingredients from the RAN and to look its action. The present objective is to validate the screening of precocious anaphase and analysis of expression of Securin and p53 in non-target cells like human peripheral blood lymphocytes (PBLs) and mouse bone marrow cells (BMCs) as early indicative parameters of RAN + lime-induced cancers. A total of 35 mice were examined at different time points for following ad libitum administration of RAN extract in drinking water with lime. Peripheral blood was collected from 32 human donors of which, 24 were RAN + lime heavy chewers. Expression of genes was assessed by immunoblotting and/or by immunohistochemistry. Histological preparation of stomach tissue of mice revealed that RAN + lime induced stomach cancer. A gradual increase in the frequency of precocious anaphases and aneuploid cells was observed in both RAN + lime-treated mouse BMC and human PBL of RAN heavy chewers. Levels of p53 and Securin were increased in these cells during early days of RAN + lime exposure. The level of Securin was significantly higher in human tumour samples than their adjacent normal counterpart. The expression of Securin was increased significantly in RAN + lime-administered mice as well as in stomach tumour. Present study revealed that precocious anaphase and expression of p53 and Securin in non-target cells are significantly associated with an increased risk of RAN-induced cancer and thus these parameters can be of early diagnostic value.

Distinct involvement of 9p21-24 and 13q14.1-14.3 chromosomal regions in raw betel-nut induced esophageal cancers in the state of Meghalaya, India.

BACKGROUND: Raw betel nut (RBN) chewing is an important contributing factor for esophageal squamous cell carcinoma (ESCC), although associated genomic changes remain unclear. One difficulty in assessing the effects of exclusively RBN induced genetic alterations has been that earlier studies were performed with samples of patients commonly using tobacco and alcohol, in addition to betel-quid. Both CDKN2A (at 9p21) and Rb1 gene (at 13q14.2) are regarded as tumor suppressors involved in the development of ESCC. Therefore, the present study aimed to verify the RBN's ability to induce ESCC and assess the involvement of CDKN2A and Rb1 genes. METHODS: A panel of dinucelotide polymorphic markers were chosen for loss of heterozygosity studies in 93 samples of which 34 were collected from patients with only RBN-chewing habit. Promoter hypermethylation was also investigated. RESULTS: Loss in microsatellite markers D9S1748 and D9S1749, located close to exon 1ß of CDKN2A/ARF gene at 9p21, was noted in 40% ESCC samples with the habit of RBN-chewing alone. Involvement of a novel site in the 9p23 region was also observed. Promoter hypermethylation of CDKN2A gene in the samples with the habit of only RBN-chewing alone was significantly higher (p=0.01) than Rb1 gene, also from the samples having the habit of use both RBN and tobacco (p=0.047). CONCLUSIONS: The data indicate that the disruption of 9p21 where CDKN2A gene resides, is the most frequent critical genetic event in RBN-associated carcinogenesis. The involvement of 9p23 as well as 13q14.2 could be required in later stages in RBN-mediated carcinogenesis.