Automatic Detection and Segmentation of Colorectal Cancer with Deep Residual Convolutional Neural Network.

Early and automatic detection of colorectal tumors is essential for cancer analysis, and the same is implemented using computer-aided diagnosis (CAD). A computerized tomography (CT) image of the colon is being used to identify colorectal carcinoma. Digital imaging and communication in medicine (DICOM) is a standard medical imaging format to process and analyze images digitally. Accurate detection of tumor cells in the complex digestive tract is necessary for optimal treatment. The proposed work is divided into two phases. The first phase involves the segmentation, and the second phase is the extraction of the colon lesions with the observed segmentation parameters. A deep convolutional neural network (DCNN) based residual network approach for the colon and polyps' segmentation from the CT images is applied over the 2D CT images. The residual stack block is being added to the hidden layers with short skip nuance, which helps to retain spatial information. ResNet-enabled CNN is employed in the current work to achieve complete boundary segmentation of the colon cancer region. The results obtained through segmentation serve as features for further extraction and classification of benign as well as malignant colon cancer. Performance evaluation metrics indicate that the proposed network model has effectively segmented and classified colorectal tumors with dice scores of 91.57% (on average), sensitivity = 98.28, specificity = 98.68, and accuracy = 98.82.

Single stage management of Gustilo type III A/B tibia fractures: Fixed with nail & covered with fasciocutaneous flap.

PURPOSE: To evaluate the role of immediate and definitive management of Gustilo type III A/B tibia fractures with intramedullary nailing and fasciocutaneous flap. METHODS: From August 2010 to July 2012, 22 patients with Gustilo Grade III A/B tibia fractures were managed with a single stage treatment of ipsilateral fasciocutaneous flap & reamed intramedullary nailing and were included in the study. The severity of the injury was calculated with Ganga Hospital injury severity score. RESULTS: The mean age of patients was 41 years and the follow-up time ranged from six months to one year. Among the 22 patients, 73% were type III B fractures with upper leg involved in 55% of them. The time interval from injury to completion of surgery was 8-14 h. The incidence of bone infection requiring secondary procedure was 9%; the major and minor soft tissue complication rate was 9% and 14% respectively. The limb salvage rate was 100%. CONCLUSION: Multidisciplinary management of severe lower limb trauma is important and provides good outcomes. Intramedullary nailing and immediate flap fixation can achieve early bone union and good soft tissue coverage, leading to good outcomes in patient with Grade III A & B tibia fractures.

Influence of plant growth stage on the essential oil content and composition in Davana (Artemisia pallens wall.).

The influence of three plant growth stages (full emergence of flower heads, anthesis, and initiation of seed set) on the essential oil content and composition in Davana (Artemisia pallens Wall) was investigated over two successive seasons. The essential oil content was found to be higher at the full emergence of flower heads than at anthesis and initiation of seed set stages. The contents of davanone, the major constituent of davana oil, and linalool decreased while those of (Z)- and (E)-methyl cinnamate, (E)-ethyl cinnamate, bicyclogermacrene, davana ether, 2-hydroxyisodavanone, and farnesol increased from flower heads emergence stage to the initiation of seed set stage. These results support the general practice of harvesting the crop at full bloom stage. Five compounds, viz., (Z)- and (E)-methyl cinnamates, (Z)- and (E)-ethyl cinnamates, and geranyl acetate, were identified for the first time in davana oil.

Cloning and developmental expression of the murine homolog of the acute leukemia proto-oncogene AF4.

AF4 is the 4q21 gene involved in the acute lymphoblastic leukemia associated t(4;11)(q21;q23) where it forms a fusion gene with MLL. In order to gain insight into AF4's role in leukemogenesis we have studied its functional domains and expression pattern during murine development. We have cloned the murine homolog, Af4. We have demonstrated that 5' half of Af4 encodes a region with transcriptional transactivation activity which is disrupted by the t(4;11) in human leukemias. We have also localized the murine AF4 protein to the nucleus supporting a role for AF4 in transcription. The developmental expression pattern of Af4 was determined in situ hybridization and suggests Af4 plays an important role in the development of the hematopoietic, cardiovascular, skeletal and central nervous systems. A repeating pattern of Af4 expression in development is down-regulation with differentiation of a tissue. Among the cell types where this pattern of down-regulation is noted are B-lymphocytes. These findings raise the possibility that the disruption of normal AF4 function by the translocation may contribute to leukemogenesis.

Inhibitors of angiotensin-converting enzyme modulate mitosis and gene expression in pancreatic cancer cells.

The angiotensin-converting enzyme (ACE) inhibitor captopril inhibits mitosis in several cell types that contain ACE and renin activity. In the present study, we evaluated the effect of the ACE inhibitors captopril and CGS 13945 (10(-8) to 10(-2) M) on proliferation and gene expression in hamster pancreatic duct carcinoma cells in culture. These cells lack renin and ACE activity. Both ACE inhibitors produced a dose-dependent reduction in tumor cell proliferation within 24 hr. Captopril at a concentration of 0.36 mM and CGS 13945 at 150 microM decreased cellular growth rate to approximately half that of the control. Neither drug influenced the viability or the cell cycle distribution of the tumor cells. Slot blot analysis of mRNA for four genes, proliferation associated cell nuclear antigen (PCNA), K-ras, protein kinase C-beta (PKC-beta) and carbonic anhydrase II (CA II) was performed. Both ACE inhibitors increased K-ras expression by a factor of 2, and had no effect on CA II mRNA levels. Captopril also lowered PCNA by 40% and CGS 13945 lowered PKC-beta gene expression to 30% of the control level. The data demonstrate that ACE inhibitors exhibit antimitotic activity and differential gene modulation in hamster pancreatic duct carcinoma cells. The absence of renin and ACE activity in these cells suggests that the antimitotic action of captopril and CGS 13945 is independent of renin-angiotensin regulation. The growth inhibition may occur through downregulation of growth-related gene expression.

Transformation of hamster pancreatic duct cells by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), in vitro.

The tobacco specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a potent carcinogen in laboratory animals. In the present study, in vitro transformation of spontaneously immortal hamster pancreatic duct cells following exposure to 20 mM NNK for 1,3,5 and 7 days is described. NNK imparted a dose-dependent and time-dependent toxicity to pancreatic duct cells in vitro. After NNK treatment, duct cells were grown either in complete duct medium (CDM) or in the absence of bovine pituitary extract, epidermal growth factor and Nu-serum (incomplete duct medium, IDM). Addition of NNK to the culture for 1 and 3 days did not affect the growth of the cells, whereas exposure of the cells for 5 and 7 days was inhibitory. One and 3 day NNK-treated cells were able to grow in the absence of growth factors and serum immediately after the treatment without any inhibition of growth. Untreated cells grew as a monolayer consisting of tightly packed polygonal cells with single nuclei. NNK treated cells also grew as a monolayer with numerous mitotic figures and multi-nucleated large cells. The doubling time between the untreated (16 h) and NNK-treated cells (14 h) was not significantly different prior to injection into the nude mice. NNK treated cells grown in IDM displayed anchorage independency in soft-agar. The tumorigenicity of the untreated and NNK treated cells (5 x 10(6)) was determined in nude mice. One and 3 day NNK-treated cells grown in CDM produced well-differentiated, mucinous tumors with a lower frequency (2/4 sites) and longer duration, but produced tumors at a higher frequency (4/4 sites) and shorter duration when grown in IDM. Five and 7 day NNK-treated cells grown in CDM did not produce any tumors; however, they produced tumors when grown in CDM followed by IDM (5/8 and 6/8 sites) with a shorter duration in nude mice. Analysis of DNA for k-ras mutation at codons 12, 13 and 61 showed G-A transition at codon 12 of the k-ras oncogene in tumor cells of 1 and 3 day NNK treatment. No mutation was detected in tumor cells from 5 and 7 day treatment.

Metabolism and activation of pancreas specific nitrosamines by pancreatic ductal cells in culture.

Metabolism of 14C labeled N-nitrosobis(2-oxopropyl)amine (BOP), N-nitroso(2-hydroxypropyl)(2-oxopropyl)amine (HPOP) and N-nitrosobis(2-hydroxypropyl)amine (BHP) by pancreatic duct cells in culture involves the following two pathways: reduction or oxidation reactions at the beta-carbon which result in the inter-conversion of these nitrosamines and activation reactions which result in the decomposition of the nitrosamine, the evolution of 14CO2 and the labeling of macromolecules. Reduction of BOP to HPOP seems to contribute significantly to the metabolism of the former nitrosamine by pancreatic duct cells, however, redox reactions at the beta-carbon of HPOP or BHP are not extensive. In terms of DNA damage, all three nitrosamines yield methyl and hydroxypropyl adducts. As expected, HPOP and BHP yield higher levels of O6-hydroxypropylguanine than BOP, while the latter yields higher levels of O6-methylguanine. There is no correlation between the ability of these nitrosamines to alkylate duct cell DNA in vitro and their carcinogenic potency in vivo. Concentrations of DNA adducts induced by pancreas specific nitrosamines (PSNs) in cultured duct cells at concentrations comparable to those found in the pancreatic juice of animals treated with BOP, are almost an order of magnitude lower than those induced in the pancreas of such animals. Discrepancies between in vitro and in vivo formation of active metabolites and DNA adducts may be attributed to the decline of the cells' ability to activate PSNs during culturing. In the same vein, the ductal cell may not be the main source of active metabolites targeting its DNA in the animal model.