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Background Pancreatic cancer is one of the most lethal diseases with an incidence almost equal to the mortality. In addition to having genetic causes, cancer can also be considered an epigenetic disease. DNA methylation is the premier epigenetic modification and patterns of aberrant DNA methylation are recognized to be a common hallmark of human tumor. In the multistage carcinogenesis of pancreas starting from precancerous lesions to pancreatic ductal adenocarcinoma (PDAC), the epigenetic changes play a significant role. Data sources Relevant studies for this review were derived via an extensive literature search in PubMed via using various keywords such as pancreatic ductal adenocarcinoma, precancerous lesions, methylation profile, epigenetic biomarkers that are relevant directly or closely associated with the concerned area of our interest. The literature search was intensively done considering a time frame of 20 years (1998–2018). Result In this review we have highlighted the hypermethylation and hypomethylation of the precancerous PDAC lesions (pancreatic intra-epithelial neoplasia, intraductal papillary mucinous neoplasm, mucinous cystic neoplasm and chronic pancreatitis) and PDAC along with the potential biomarkers. We have also achieved the early epigenetic driver that leads to progression from precancerous lesions to PDAC. A bunch of epigenetic driver genes leads to progression of precancerous lesions to PDAC (ppENK, APC, p14/5/16/17, hMLH1 and MGMT) are also documented. We summarized the importance of these observations in therapeutics and diagnosis of PDAC hence identifying the potential use of epigenetic biomarkers in epigenetic targeted therapy. Epigenetic inactivation occurs by hypermethylation of CpG islands in the promoter regions of tumor suppressor genes. We listed all hyper- and hypomethylation of CpG islands of several genes in PDAC including its precancerous lesions. Conclusions The concept of the review would help to understand their biological effects, and to determine whether they may be successfully combined with other epigenetic drugs. However, we need to continue our research to develop more specific DNA-demethylating agents, which are the targets for hypermethylated CpG methylation sites.

Since ensuring stability of the nanoparticles in aqueous-phase is essential for biomedical applications, this study evaluated the effect of ultra-sonication followed by peptization on iron-oxide na...

BackgroundPancreatic ductal adenocarcinoma (PDAC) is one of the leading cancers worldwide and has a poor survival, with a relative five-year survival rate of only 8.5%. In this study we investigated epigenetic marksassociated with PDAC severity and prognosis, through studying alterations in DNA methylation patterns.MethodsDNA methylome for tumor and adjacent normal tissue samples from PDAC patients (n=7) were generated using Illumina 450K bead chips. Differentially methylated positions (DMPs) were identified with |delta beta| > 0.2 and p-valueResultsWe identified 76 DMPs in PDAC patients that mapped to 43 genes. Among them, 44.7% (n=34) were hypo-methylated and 55.3% (n=42) were hyper-methylated DMPs in cancer samples. The trends of change in methylation at these 76 DMPs from well to moderate were like that from moderate to poorly differentiated cancer samples. The gradual trend in differential methylation was observed both in our cohort and the TCGA-PAAD cohort, suggesting methylation marks can serve as early indicators of disease pathology. Altered promoter methylation, which may affect gene expression, was observed for transcription regulators (BHLHE23, GSC2, FOXE1 and TWIST1), gated ion channels (KCNA6, and CACNB2), tumor suppressors (RASSF1, SPRED2, and NPY) and genes functioning in interferon signalling (SIGIRR, MX2, and OAS2). We also have compared the TCGA-PAAD dataset with normal pancreatic tissue data from GTEx V8 dataset leading to a confluent observation.ConclusionsWe reported the first study on methylome in PDAC tumors from patients in India. We identified altered DNA methylation associated with increasing severity in PDAC among some genes like SIGIRR, MX2 along with other previously reported loci. We also concluded a confluence in our observation when comparing the TCGA-PAAD dataset with GTEx V8 dataset.

Background Pancreatic Ductal Adenocarcinoma (PDAC) is a cancer of the exocrine pancreas and 5-year survival rates remain constant at 7%. Along with PDAC, Periampullary Adenocarcinoma (PAC) accounts for 0.5–2% of all gastrointestinal malignancies. Genomic observations were well concluded for PDAC and PACs in western countries but no reports are available from India till now. Methods Targeted Next Generation Sequencing were performed in 8 (5 PDAC and 3 PAC) tumour normal pairs, using a panel of 412 cancer related genes. Primary findings were replicated in 85 tumour samples (31 PDAC and 54 PAC) using the Sanger sequencing. Mutations were also validated by ASPCR, RFLP, and Ion Torrent sequencing. IHC along with molecular dynamics and docking studies were performed for the p.A138V mutant of TP53. Key polymorphisms at TP53 and its associated genes were genotyped by PCR-RFLP method and association with somatic mutations were evaluated. All survival analysis was done using the Kaplan-Meier survival method which revealed that the survival rates varied significantly depending on the somatic mutations the patients harboured. Results Among the total 114 detected somatic mutations, TP53 was the most frequently mutated (41%) gene, followed by KRAS, SMAD4, CTNNB1, and ERBB3. We identified a novel hotspot TP53 mutation (p.A138V, in 17% of all patients). Low frequency of KRAS mutation (33%) was detected in these samples compared to patients from Western counties. Molecular Dynamics (MD) simulation and DNA-protein docking analysis predicted p.A138V to have oncogenic characteristics. Patients with p.A138V mutation showed poorer overall survival (p = 0.01). So, our finding highlights elevated prevalence of the p53p.A138V somatic mutation in PDAC and pancreatobiliary PAC patients. Conclusion Detection of p.A138V somatic variant in TP53 might serve as a prognostic marker to classify patients. It might also have a role in determining treatment regimes. In addition, low frequency of KRAS hotspot mutation mostly in Indian PDAC patient cohort indicates presence of other early drivers in malignant transformation.

Additional file 2. Supplemental methods.

Additional file 7.

Additional file 1: Fig. 1. Hematoxilin and Eosin (H&E) staining of types of tumors. a. H&E staining of a PDAC tumor (left 10x magnification, right 20x magnification). b. H&E staining of an intestinal type of PAC tumor (left 10x magnification, right 20x magnification). c. H&E staining of a pancreatobiliary type of PAC tumor (left 10x magnification, right 20x magnification). Fig. 2. Validation of selected variants. Few of the somatic mutations identified in NGS study are being validated by Sanger sequencing method. Validated nucleotides are marked by vertical lines, in each pair upper one is for tumor DNA and lower one is for normal tissue or blood DNA. Fig. 3. Signature of somatic mutations identified in total patient cohort (n = 93). a. In the X axis different types of mutations is given and Y axis denoting frequency of types of mutations. b. Transition and transversion ration of all point mutations. c. In X axis six different signatures of point mutations is given and Y axis denoting the frequency of different signatures. Fig. 4. Frequency of mutations in other recurrently mutated genes in all patients. Different functional domains of proteins are indicated by different colours. The Y axis denotes frequency of mutations and X axis denotes mutations in different positions of the protein domains. Each vertical bar indicates mutation . Recurrent mutations are marked with red circle a.KRAS mutations.b. SMAD4 mutations. c. CTNNB1 mutations. Fig. 5. Damaging and pathogenic variants of non synonymous mutations (n = 57). Damaging and pathogenic variants of non synonymous mutations (n = 57). The dark ass coloured boxes indicates mutations identified as damaging by different functional prediction tools (Provean, SIFT, and Mutation Assessor). The white coloured boxes mean the tolerated mutations whereas light grey coloured boxes mean “unable to identify”. All the dark grey coloured boxes in the ClinVar_Status row indicate pathogenic or likely pathogenic variants and black coloured boxes are reported as uncertain significance in ClinVar database. Fig. 6. Comparison of reported and novel variants observed in this study with those reported in TCGA and Cosmic database. These are the total mutations identified by both NGS and Sanger sequencing method. The blue coloured boxes in sample row are PAC mixed samples, Sky coloured boxes are PAC intestinal samples, Grey coloured boxes are PAC pancreatobiliary samples and yellow coloured boxes are PDAC samples. The red colouredboxes in COSMIC and TCGA row are the reported mutation in these databases. The boxes marked with “×” in TCGA_PDAC row are not compared as these are PAC mutations data. Among the PDAC samples, red coloured boxes are the mutations which were also observed in TCGA_PDAC (n = 185) mutation data. Fig. 7. Detection of KRAS and TP53 p.A138V mutations by allele specific PCR (a-f). Fig. 8.KRAS 12th codon mutation detection by PCR-RFLP method. Lane 1 represent 100 bp DNA ladder. Lane 2 to 11 represents tumour normal paired samples. Mutant samples can be differentiate with presence of 197 fragments in T1, T2, T3, and T5 as BstNI cannot digest mutant containing fragment. Here sample T4-N4 pair is negative control and T5-N5 pair is positive control of NGS cohort. Fig. 9.KRAS mutation screening by different methods in PDAC samples. First row indicates KRAS mutation status in 36 PDAC samples. The yellow colour indicates G12D mutations, violate colour indicates G12V mutation, sky colour indicates Q61H mutation, green colour indicates G12A mutation, no colour boxes indicate samples with no mutation, and light grey colour indicates samples with failed amplification or poor sequence quality. Other rows indicate different methods (Sanger sequencing, ASPCR, and PCR-RFLP) used for KRAS mutation detection. In the methods rows, red colour indicates identification of mutation, white colour indicates mutations could not be identified, and dark ash colour indicates not applicable due to PCR failure for those samples. Fig. 10. Identification of p.A138V mutation in TP53 gene by Sanger sequencing. The p.A138V mutation in TP53 identified in 16 patients. Here showing two chromatogram (a&b) for p.A138V (Vertical line indicates C/T heterozygous peak) variant identified by Sanger sequencing in 2 patients in the tumour but absent in corresponding normal. Fig. 11. Comparison SSE plots between wild type TP53and A138Vmut TP53. Fig. 12. Intermolecular hydrogen bonding analysis between TP53 (DBD) and DNA complex with respect to wild type and A138Vmut TP53 protein. Number of intermolecular hydrogen bonds between TP53(DBD) (wild type and mutant) and DNA represented in a multivariate plot which shows greater density of data points at 8–12 in wild type (left) and in 5–10 for the mutant (right). Therefore, greater number of intermolecular hydrogen bonds prevailed in the wild type DBD-DNA dynamics simulation than in the corresponding mutant DBD-DNA. Fig. 13. Copy number variation plot for ERBB2 in 93 patients. “X” axis denotes two groups of tissues (Normal and Tumour) of all patients whereas “Y” axis indicates fold change (2-ΔCT) of respective groups. Fig. 14.KRAS hotspot region of 8 tumor samples studied by NGS. Showing reads of KRAS gene focusing on hotspot codon 12 of 8 samples (a-h). Integrative Genomic Browser (IGV) was used for visualization of reads. In figures,“a-h” except “e”, only “C” allele is present in the particular position of KRAS gene, whereas figure“e” indicated “C” and mutant “G” alleles in same position. In figure e the variant allele “G” is represented by orange coloured on the reads. Fig. 15. Comparison of overall survival of p.A138V mutant vs. other TP53 hotspot mutants of TCGA PDAC cohort. Kaplan-Meier survival analysis of all TP53 hotspot mutants of TCGA PDAC cohortalong with TP53 A138V mutants of our patient.

Additional file 9.

Pancreatic Ductal AdenoCarcinoma (PDAC) is one of the most lethal malignancies of all solid cancers. Precancerous lesions for PDAC include PanIN, IPMNs and MCNs. PDAC has a poor prognosis with a 5-year survival of approximately 6%. Whereas Periampulary AdenoCarcinoma (PAC) having four anatomic subtypes, pancreatic, Common Bile Duct (CBD), ampullary and duodenum shows relative better prognosis. The highest incidence of PDAC has been reported with black with respect to white population. Similarly, incidence rate of PAC also differs with different ethnic populations. Several lifestyle, environmental and occupational exposures including long-term diabetes, obesity, and smoking, have been linked to PDAC, however, for PAC the causal risk factors were poorly described. It is now clear that PDAC and PAC are a multi-stage process resulting from the accumulation of genomic alterations in the somatic DNA of normal cells as well as inherited mutations. Approximately 10% of PDAC have a familial inheritance. Germline mutations in CDKN2A, BRCA2, STK11, PALB2, PRSS1, etc., as well as certain syndromes have been well associated with predisposition to PDAC. KRAS, CDKN2A, TP53 and SMAD4 are the 4 “mountains” (high-frequency driver genes) which have been known to earliest somatic alterations for PDAC while relatively less frequent in PAC. Our understanding of the molecular carcinogenesis has improved in the last few years due to extensive research on PDAC which was not well explored in case of PAC. The genetic alterations that have been identified in PDAC and different subgroups of PAC are important implications for the development of genetic screening test, early diagnosis, and prognostic genetic markers. The present review will provide a brief overview of the incidence and prevalence of PDAC and PAC, mainly, increased risk in India, the several kinds of risk factors associated with the diseases as well as required genetic alterations for disease initiation and progression.

This paper reports the design, fabrication, and testing of a microfluidic MEMS biosensor for rapid sensing of low concentration

Diabetes insipidus is a disease charaterised by increased urine production and thrist. Neurogenic diabetes insipidus following head trauma,autoimmune disease and infection is quite common but diabetes insipidus following thermal burn injury is a rare complication.We should know about this complication as its management need a comprehensive approach for satisfactory outcome. Thermal burn can cause different complications in early post burn period like electrolyte imbalance, dehydration, acute renal failure, but diabetes insipidus is a very rare and unusual complication that may come across in thermal burn. We should be aware about this condition to prevent and treat mortality and morbidity in burn patients. We have reported a case of transient diabetes insipidus in a patient of thermal burn in early post burn period. Patient was treated accordingly, leading to complete recovery.

A MEMS-based impedance biosensor was designed, fabricated, and tested to effectively detect the presence of bacterial cells including E. coli O157:H7 and Salmonella typhimurium in raw chicken products using detection region made of multiple interdigitated electrode arrays. A positive dielectrophoresis based focusing electrode was used in order to focus and concentrate the bacterial cells at the centerline of the fluidic microchannel and direct them toward the detection microchannel. The biosensor was fabricated using surface micromachining technology on a glass substrate. The results demonstrate that the device can detect Salmonella with concentrations as low as 10 cells/mL in less than 1 h. The device sensitivity was improved by the addition of the focusing electrodes, which increased the signal response by a factor between 6 and 18 times higher than without the use of the focusing electrodes. The biosensor is selective and can detect other types of pathogen by changing the type of the antibody immobilized on the detection electrodes. The device was able to differentiate live from dead bacteria.

This paper reports the design, fabrication and characterization of an impedance based biosensor for simultaneous detection of three Salmonella serogroups (type B, D, and E), with low concentration in ready to eat Turkey matrix. The measurements demonstrate that the device can selectively detect Salmonella, e.g., type B at a concentration as low as 8 cell/ml with a detection time of 1 hour. The addition of focusing region has improved the signal strength by a factor ranged between 4. The antibody immobilization on top of the detection electrodes was studied as a function of time between 0.5 - 3 hours. The results demonstrate that an optimized coating can be achieved within 1.5 hours at 1X antibody coating. The design has shown a significant improvement in capability to detect Salmonella compared to traditional culture methods, PCR and ELISA based detection.

This paper reports the design, fabrication, and testing of a microfluidic MEMS biosensor for rapid sensing of low concentration Escherichia coli O157:H7. It consists of a specially designed focusing and sensing region, which enables the biosensor to detect low concentration of bacterial cells. The focusing region consists of a ramped vertical electrode pair made of electroplated gold along with tilted thin film finger pairs (45°) embedded inside a microchannel. The focusing region generates positive dielectrophoresis force, which moves the cells towards the edges of the tilted thin film electrode fingers, located at the center of the microchannel. The fluidic drag force then carries the focused cells to the sensing region, where three interdigitated electrode arrays (IDEAs) with 30, 20, and 10 pairs, respectively, are embedded inside the microchannel. This technique resulted in highly concentrated samples in the sensing region. The sensing IDEAs are functionalized with the anti-E. coli antibody for specific sensing of E. coli 0157:H7. As E. coli binds to the antibody, it results in an impedance change, which is measured across a wide frequency range of 100 Hz–10 MHz. The biosensor was fabricated on a glass substrate using the SU8 epoxy resist to form the microchannel, gold electroplating to form the vertical focusing electrode pair, a thin gold film to form the sensing electrode, the finger electrodes, traces and bonding pads, and polydimethylsiloxane to seal the device. The microfluidic impedance biosensor was tested with various low concentration bacterial samples and was able to detect bacterial concentration, as low as 39 CFU/ml with a total sensing time of 2 h.

Gallbladder carcinoma (GBC) is the most common malignant tumor of the biliary tract throughout the world with marked ethnic and geographical variations. GBC is the highly fatal disease with poor prognosis. GBC appears to develop dysplastic mucosa that progress to carcinoma in situ and then to invasive carcinoma. The incidence of GBC varies geographically with higher rates in certain areas of Latin America (Columbia, Peru and Ecuador), North America (Hispanic and American Indian populations) Eastern Europe (Poland, the Czech Republic, Slovakia, Hungary, and the former East Germany) and Japan. Mapuche Indians of Chile show the highest incidence and mortality of GBC. In India, GBC is more common in women in the North, North-East and East compared to the Southern part, The incidence of GBC is very high in the northern cities like Uttar Pradesh, Bihar, Orissa, West Bengal and Assam (e.g. in Delhi it is 4.5 per 100,000 for men and 10.1 per 100,000 for women) compared with the southern cities (in Chennai, Mumbai, Trivandrum, and Bangalore) incidence is 1.2 per 100,000 for men and 0.9 per 100,000 in women. Cholelithiasis/gallstones are found in 65-90% of patients with GBC. Apart from gallstones and gender biasness, a number of other risk factors favor the development of GBC like obesity, reproductive factors, genetic susceptibility, ethnicity, chronic infections and inflammations and environmental exposures to specific chemicals. Elucidating such risk factors not only provides insight into its pathogenesis accounting for its geographic and ethnic variances, but more importantly should yield strategies to prevent and treat this unusual malignancy.

We present a low cost, easy to fabricate biosensor, which can quickly and accurately detectSalmonella typhimurium. This study also compares the advantages of the microfluidic biosensor over a nonmicrofluidic biosensor. High density interdigitated electrode array was used to detectSalmonellacells inside a microfluidic chip. Monoclonal anti-Salmonellaantibodies were allowed to be immobilized on the surface of the electrode array for selective detection ofSalmonella typhimurium. An impedance analyzer was used to measure and record the response signal from the biosensor. The biosensor provides qualitative and quantitative results in 3 hours without any enrichment steps. The microfluidic biosensor’s lower detection limit was found to be3×103 CFU/mL compared to the3×104 CFU/mL of the nonmicrofluidic biosensor, which shows that the microfluidic biosensor has 10-fold increased sensitivity. The impedance response of microfluidic biosensor was also significantly higher (2 to 2.9 times) compared to the nonmicrofluidic biosensor.

Introduction: Pancreatic Ductal Adenocarcinoma (PDAC), the most common primary malignant disease of the pancreas and the periampullary region, accounts for about 75% of all nonendocrine tumors arising in this region. It is 4th most lethal malignancies. The 5 year survivability rate is below 5%. At the beginning of the 21st century, the estimated number of PC worldwide was 110,000, with an estimated global mortality rate of 98%. Incidence of periampullary adenocarinoma (PACs) is low, approximately 0.5-2% of all gastrointestinal malignancies and 20% of all tumors of the extrahepatic biliary tree. Aims & Objectives: To identify the somatic single nucleotide variants (SNV’s) in 412 cancer related genes in PDAC & PAC’s. To identify possible altered biological pathways enriched in these cancers. Methodology: DNA samples from Tissue and blood were sequenced for exon sequencing of 412 cancer related genes (NIMBLGNE panel, Custom). Raw fastq files processed using GATK tools and variants identified by Varscan2, & MuTect. Altered pathways identified by KEEG. Result: A total 105 Somatic exonic Single Nucleotide Variants (SNV’s), 9 somatic exonic Indels, 22 LOH mutations (both Indel and SNV’s) were identified in our sample set. Among the candidate genes of PDAC somatic SNV’s were found in TP53, SMAD4 in some patient whereas frequency of KRAS mutation was less frequent. Fourteen SNV’s were reported in cosmic database which includes 5 pathogenic variants, whereas 91 SNV’s were novel. A total 75 non-synonymous, 6 stopgain, and 24 synonymous SNV’s were observed among 105 SNV’s. Fifty eight percent of transversion and 52% of transition observed from all SNVs. Among all transversion fifty five percent SNV’s were C>T, G>T. PI3-Akt, Proteoglycans in cancer, Transcription misregulation, Rap1, ErbB, Neurotrophin pathways were found to be most commonly enriched in our patient population. Our data strongly suggest PI3-Akt, Proteoglycans in cancer pathways play a critical role in the disease. Conclusion: This study implicates a landscape of somatic SNV’s in PDAC’s and PAC’s and alteration of biological pathways in our patient population. We also observeed ERBB2 and KMT2C genes are predominantly alerted in PDAC’s and PAC’s. P53, KRAS and SMAD4 are the known mutated genes contributes very similar mutational pattern. Citation Format: Nilabja Sikdar, Gourab Saha, Richa Singh, Dhiraj Anchlia, Paromita Roy, Supriyo Ghatak, Sudeep Banerjee, Sumit Gulati, Shibajyoti Ghosh. Somatic genomic alteration of 412 cancer-targeted genes of periampullary and pancreatic ductal adenocarcinoma in Indian patient population [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4395. doi:10.1158/1538-7445.AM2017-4395

We report an interdigitated electrode array (IDEA) impedance biosensor with rapid detection of Escherichia coli O157:H7. This biosensor has significantly better detection capability compared with the conventional microbiological testing method. The total detection time for this biosensor is under 3 hours. Dielectrophoresis (DEP) is used in conjunction with impedance spectroscopy to improve the detection capability of the biosensor. The IDEA surface is functionalized using anti-E.coli antibody for selectivity of the bacteria. The dose response was in-between 3 × 106 CFU/mL and 3 × 102 CFU/mL. This is 10 fold better than the detection limit previously reported using impedance based biosensors.

An impedance biosensor was designed, fabricated and tested for detection of viable Escherichia coli O157:H7 in food samples. This device consists of interdigitated microelectrode array (IDEA) fabricated using thin layer of sputtered gold, embedded under a polydimethylsiloxane (PDMS) microchannel. The array of electrodes is designed to detect viable EColi in different food products. The active surface area of the detection array was modified using goat anti-E.coli polyclonal IgG antibody. Contaminated food samples were tested by infusing the supernatant containing bacteria over the IDEA's, through the microchannel. Antibody-antigen binding on the electrodes results in impedance change. Four serial concentrations of E.coli contaminated food samples (3x102 CFUmL-1 to 3x105 CFUmL-1) were tested. The biosensor successfully detected the E.coli samples, with the lower detection limit being 3x103 CFUmL-1 (up to 3cells/μl). Comparing the test results with an IDEA impedance biosensor without microchannel (published elsewhere) indicates that this biosensor have two order of magnitude times higher sensitivity. The proposed biosensor provides qualitative and quantitative detection, and potentially could be used for detection of other type of bacteria by immobilizing the specific type of antibody.© (2012) COPYRIGHT Society of Photo-Optical Instrumentation Engineers (SPIE). Downloading of the abstract is permitted for personal use only.

A gold interdigitated microelectrode (IME) impedance biosensor was fabricated for the detection of viable Escherichia coli O157:H7 . This sensor was fabricated using lithography techniques. The surface of the electrode was immobilized with anti- E. coli IgG antibodies. This approach is different from other studies where the change in impedance is measured in terms of growth of bacteria on the electrode, rather then the antibody/antigen bonding. The impedance values were recorded for frequency ranges between 100 Hz and 10 MHz. The working range of the dose response for this device was found to be between 2.5 × 10 4 CFU ml −1 and 2.5 × 10 7 CFU ml −1 . The time response studies indicated that antibody/antigen binding is not a function of time, but can decrease if excess times are allowed for binding. It was observed that the impedance values for 60 min antibody/antigen binding were higher than the impedance values for 120 min binding time. The main advantages of the reported device are that, it provides for both qualitative and quantitative detection in 3 h while other impedance sensors reported earlier may take up to 24 h for detection. If enrichment steps are required then it may take 3–4 days to infer the results. This sensor can be used to detect different types of bacteria by immobilizing the antigen specific antibody. Most of the sensors are not reusable since they either use enzymes or enrichment steps for detection but this device can be reused, following a cleaning protocol which is easy to follow. Each device was used at least five times. The simplicity of this sensor and the ease of fabrication make this sensor a useful alternate to the microfluidics and enzyme based impedance sensors, which are relatively more difficult to fabricate, need programmable fluidic injection pumps to push the sample through the channel, suffer from limitation of coagulation and are difficult to clean.

Gastric tuberculosis is an extremely rare entity particularly when it is not associated with pulmonary tuberculosis or an immunodeficient state. Here one patient required surgery for gastric outlet obstruction and was subsequently put on antituberculous drugs. The patient responded well to treatment and is currently doing well in follow-up. This disease though rare should be considered in the differential diagnosis of gastric malignancy and severe peptic ulcer disease.

It was a common belief that cancer is more prevalent among the lower socio-economic group. It was also generally accepted that mortality was higher in this group due to various reasons. In this hospital based study, an attempt had been made to find out any association between cancer incidence and socio-economic factors like age, sex, education, occupation, and income. The relative distribution of cancers in different parts of the body was also analysed. Collected data for cancers of the breast, lung, cervix and gall bladder were also analysed separately. It was found that there was a significant association between the occurrence of cancer and the middle income group earning Rs 12000-60000 annually. On the other side people having higher education and higher income were less likely to suffer from cancer and presented at an earlier stage.

Penetrating trauma to neck resulting in arteriovenous (AV) fistula and aneurysms involving the carotid system are uncommon injuries with life-threatening consequences. We report here a case of a young factory worker who developed a traumatic AV fistula with false aneurysm, with however, no other complications. He was successfully operated when he presented to us two months after the injury and is doing well in follow-up.

Plexiform angiomyxoid myofibroblastic tumour (PAMT) has recently emerged as a new entity among gastrointestinal mesenchymal tumours. All of the 27 cases reported until now originated from the stomach. We report the first case of a duodenal PAMT arising from the first part of the duodenum in a 19-year-old woman presenting with upper abdominal pain and an abdominal lump.

Background: The purpose of this study was to examine the feasibility of single-stage resection and anastomosis for acute left-sided colonic obstruction due to acute sigmoid volvulus without intraoperative lavage. Mechanical bowel preparation has been shown to be unnecessary for elective colorectal surgery. Colonic decompression without intraoperative lavage may simplify operations in acute left-sided colorectal obstruction. Methods: Emergency resection of acute sigmoid volvulus was performed. This was followed by primary anastomosis without on-table lavage after closed bowel decompression. Results: A total of 197 patients underwent bowel decompression, resection and primary colonic anastomosis. Two patients developed anastomosis leak, requiring re-laparotomy, Hartmann's procedure and delayed closure. Two deaths occurred postoperatively; these were unrelated to the nature of the surgery. The mean hospital stay was 9.8 days. Conclusion: Primary colonic anastomosis can be safely done for obstructed left colon due to acute sigmoid volvulus without intraoperative colonic lavage.

We report a rare case of a primary adrenal cortical malignancy presenting with spontaneous retroperitoneal haemorrhage in a young adult. To the best of our knowledge, this is the thirteenth such case to be reported in the English literature.

Feeding jejunostomy is a procedure of tremendous importance in our day-to-day practice of gastrointestinal surgery. Like any other surgical procedure, it is also associated with some common complications such as pain, infection, intra peritoneal leakage, dislodgment, strangulation, and small bowel necrosis. Small bowel intussusception is a complication of feeding jejunostomy, which is very rare and unique. We report the case of a 30-year-old female who presented with small bowel intussusceptions following feeding jejunostomy.

An impedance biosensor based on interdigitated electrode (IDE) arrays was designed, fabricated and tested for detection of Escherichia coli O157:H7. The device consists of two sets of gold IDE arrays embedded in a SU8-PDMS microchannel. The first set of electrodes uses positive dielectrophoresis (p-DEP) force to focus and concentrate the E. coli into the centre of the microchannel, and direct it towards the detection zone microchannel which has dimensions of a third of the first channel. The bulk fluid keeps flowing toward the outer channel into the waste outlets. The second sets of electrodes are located in the centre channel and are used for impedimetric detection of the E. coli. A combination of standard photolithography, wet etching and plasma treatment techniques were used to fabricate the biosensor. The E. coli cells in the test solution were focused into the centre of the channel when an excitation signal of 5 Vp–p at 5.6 MHz was applied across the electrode arrays. Before injecting the E. coli cells, polyclonal anti-E. coli antibodies were non-specifically immobilized on the sensing electrode array. This ensures specific detection of E. coli O157:H7 bacterial cells. As the concentrated E. coli cells (antigen) reach the sensing electrode array, they bind to the immobilized antibody sites. This antigen–antibody binding causes a change in the impedance, which is measured using an impedance analyzer. The device performance was tested by measuring the impedance, between 100 Hz and 1 MHz frequency, before and after applying p-DEP on the focusing electrode array, and after applying p-DEP on both the focusing and sensing electrodes. The result shows clearly that the use of p-DEP on the focusing IDE array significantly increased the measurement sensitivity with the lower detection limit being 3 × 102 CFU mL−1. In addition, the use of p-DEP on both electrode arrays increased the measurement sensitivity by a factor of 2.9 to 4.5 times depending on the concentration.

To study the feasibility of acute appendicectomy in patients with an appendicular mass.Department of Surgery, Bankura Sammalani Medical College (BSMCH), Bankura, West Bengal, India.From January 1998 to May 2001. 87 patients were diagnosed and operated for appendix mass within 24 h of admission. None of the patients had any associated complications.A McBurney's incision with Rutherford-Morrison extension was made in most patients.48 patients presented with a classical appendix mass. 25 patients (28.7%) had classical features of appendix abscess, and in 14 (16.1%) a loculated collection of pus (10 to 50 ml) was found. Operative time ranged from 45 to 90 min (mean 65). Pathologic evidence of appendicitis was present in all patients. 71 patients were discharged on the seventh postoperative day. 15 patients developed minor wound infection. One patient developed band obstruction, which subsided spontaneously on conservative treatment. Rest of the patients are doing well.Low morbidity, reduced hospital stay, low cost and patient compliance favour operative management of appendicular mass by experienced surgeons thus obviating the old practice of conservative treatment followed by interval appendicectomy.