Amelioration of immune and digestive system through weed supplemented feed against Aeromonas hydrophila in Clarias gariepinus.

Aquaculture is one of the important globally growing industries. It serves as an important food source of protein for human beings. With the expanding demand for the fish and their products it has become extremely important to improve the aquaculture practices. Aquaculture in India has witnessed huge mortalities caused by bacteria, viruses, fungi, nematodes etc. Aquatic weeds plants are harmful for aquaculture in many ways. Present study is aimed to overcome the disease caused by Aeromonas hydrophila (fish pathogenic bacteria) through feed supplementation of two aquatic weed plants (Azolla pinnata and Ceratophyllum demersum). The fish were divided into 6 groups: experimental groups (fish fed on supplementary feed at 5% and 2.5% concentration for individual plant and challenged with bacteria), positive control (fish fed on non-supplemented feed and challenged with bacteria) and negative control (fish fed on non-supplementary feed and not challenged with bacteria). It was observed that supplemented feed enhanced both cell mediated and humoral immunity in fish. Therefore, we advocate that feed formulated with incorporation of Azolla pinnata and Ceratophyllum demersum leaf powder at 5% and 2.5% could be used to prevent disease caused by A. hydrophila or can be used to enhance fish health by boosting its immune system. The results of this study also showed an improved digestibility in fish fed on supplemented feed.

Prevalence of allergic rhinitis and asthma in patients with chronic rhinosinusitis and gastroesophageal reflux disease.

BACKGROUND: An association between chronic rhinosinusitis (CRS) and gastroesophageal reflux disease (GERD) has been previously reported; however, the underlying factors linking CRS and GERD remain to be elucidated. OBJECTIVE: To assess the association of GERD and CRS using prospective and retrospective approaches. METHODS: The retrospective study comprised a large cohort of CRS cases, whereas the prospective arm evaluated a series of CRS cases and controls. RESULTS: In the retrospective arm of the study, of the 1066 patients with CRS, 112 (10.5%) had GERD. Among patients with CRS, GERD was associated with higher body mass index, older age, and female sex. The odds ratios (ORs) for asthma and allergic rhinitis in the CRS group with GERD compared with the CRS group without GERD were 2.89 (95% confidence interval [CI], 1.905-4.389) and 2.021 (95% CI, 1.035-3.947). Furthermore, GERD was associated with a greater duration of CRS. Ninety patients with CRS and 81 controls were enrolled in the prospective arm of the study. In the CRS group, GERD was associated with asthma (OR, 4.77; 95% CI, 1.27-18.01). Patients with CRS and GERD had a longer duration and a younger age at onset of CRS. In controls, no association was found between GERD and asthma (OR, 0.67; 95% CI, 0.09-5.19) or allergic rhinitis (OR, 0.35; 95% CI, 0.05-2.59). CONCLUSION: Patients with CRS and GERD are more likely to have atopic conditions and asthma when compared with patients with CRS but without GERD. One of the potential explanations of this link is that comorbid GERD and atopic disease are potential risk factors for development of CRS.

African American Patients with Chronic Rhinosinusitis Have a Distinct Phenotype of Polyposis Associated with Increased Asthma Hospitalization.

BACKGROUND: Chronic rhinosinusitis (CRS) is a common inflammatory disease of the upper airways that is often categorized into subtypes including "with" and "without" nasal polyps. However, the influence of multiple important epidemiologic factors, including race, on CRS has not been investigated. OBJECTIVE: The present study assessed various phenotypic characteristics of CRS in patients, living in the United States, with different racial backgrounds. METHODS: We performed a large retrospective cohort study of patients with CRS treated at a large urban tertiary care referral center in Chicago. RESULTS: African American (AA) patients with CRS living in Chicago were more likely to report hyposmia as a symptom of CRS. Furthermore, AA patients with CRS who failed medical therapy and required surgical intervention had a significantly higher frequency of nasal polyposis and aspirin-exacerbated respiratory disease, and a higher disease severity index on computed tomography imaging than did white patients with CRS. The increased polyposis in AAs was associated with increased hospitalization for asthma. There were no differences in the prevalence of atopy, asthma, atopic dermatitis, food allergy, duration of disease, or number of surgeries between different races. CONCLUSIONS: AAs with refractory CRS are at increased risk for nasal polyposis, smell loss, aspirin-exacerbated respiratory disease, and a greater severity of disease based on imaging, resulting in increased health care utilization.

Signaling Networks of Activated Oncogenic and Altered Tumor Suppressor Genes in Head and Neck Cancer.

Head and neck squamous cell carcinoma (HNSCC) arises from the upper aerodigestive tract and is the six most common cancers worldwide. HNSCC is associated with high morbidity and mortality, as standard surgery, radiation, and chemotherapy can cause significant disfigurement and only provide 5-year survival rates of ~50-60%. The heterogeneity of HNSCC subsets with different potentials for recurrence and metastasis challenges the traditional pathological classification system, thereby increasing demand for the development of new diagnostic, prognostic, and therapeutic tools based on global molecular signatures of HNSCC. Historically, using classical biological techniques, it has been extremely difficult and time-consuming to survey hundreds or thousands of genes in a given disease. However, the development of high throughput technologies and high-powered computation throughout the last two decades has enabled us to investigate hundreds or thousands of genes simultaneously. Using high throughput technologies, our laboratory has identified the gene signatures and protein networks, which significantly affect HNSCC malignant phenotypes, including TP53/p63/p73 family members, IL-1/TNF-ß/NF-κB, PI3K/AKT/mTOR, IL-6/IL-6R/JAK/STAT3, EGFR/MAPK/AP1, HGF/cMET/EGR1, and TGFß/TGFßR/TAK1/SMAD pathways. This review summarizes the results from high-throughput technological assays conducted on HNSCC samples, including microarray, DNA methylation, miRNA profiling, and protein array, using primarily experimental data and conclusions generated in our own laboratory. The use of bioinformatics and integrated analyses of data sets from different platforms, as well as meta-analysis of large datasets pulled from multiple publicly available studies, provided significantly higher statistical power to extract biologically relevant information. The data suggested that the heterogeneity of HNSCC genotype and phenotype are much more complex than we previously thought. Understanding of global molecular signatures and disease classification for specific subsets of HNSCC will be essential to provide accurate diagnoses for targeted therapy and personalized treatment, which is an important effort toward improving patient outcomes.

Acroangiodermatitis of mali: a rare vascular phenomenon.

Acroangiodermatitis (synonym pseudo-Kaposi sarcoma) is an unusual, benign condition which clinically presents as purple-colored patches, plaques or nodules, mostly on the extensor surfaces of lower extremities in patients with chronic venous insufficiency and arteriovenous malformations. It resembles aggressive conditions like Kaposi's sarcoma and requires histopathological examination for its diagnosis. We report two such cases of acroangiodermatitis. Histopathology of both the cases showed dilated capillaries in the dermis with extravasated red blood corpuscles (RBCs), hemosiderin deposits, and hyperplastic granulation tissue. Both were treated with oral antibiotics and topical steroids. The ulcers showed a good response within 2 months of treatment.

Analysis of albumin-associated peptides and proteins from ovarian cancer patients.

BACKGROUND: Albumin binds low-molecular-weight molecules, including proteins and peptides, which then acquire its longer half-life, thereby protecting the bound species from kidney clearance. We developed an experimental method to isolate albumin in its native state and to then identify [mass spectrometry (MS) sequencing] the corresponding bound low-molecular-weight molecules. We used this method to analyze pooled sera from a human disease study set (high-risk persons without cancer, n = 40; stage I ovarian cancer, n = 30; stage III ovarian cancer, n = 40) to demonstrate the feasibility of this approach as a discovery method. METHODS: Albumin was isolated by solid-phase affinity capture under native binding and washing conditions. Captured albumin-associated proteins and peptides were separated by gel electrophoresis and subjected to iterative MS sequencing by microcapillary reversed-phase tandem MS. Selected albumin-bound protein fragments were confirmed in human sera by Western blotting and immunocompetition. RESULTS: In total, 1208 individual protein sequences were predicted from all 3 pools. The predicted sequences were largely fragments derived from proteins with diverse biological functions. More than one third of these fragments were identified by multiple peptide sequences, and more than one half of the identified species were in vivo cleavage products of parent proteins. An estimated 700 serum peptides or proteins were predicted that had not been reported in previous serum databases. Several proteolytic fragments of larger molecules that may be cancer-related were confirmed immunologically in blood by Western blotting and peptide immunocompetition. BRCA2, a 390-kDa low-abundance nuclear protein linked to cancer susceptibility, was represented in sera as a series of specific fragments bound to albumin. CONCLUSION: Carrier-protein harvesting provides a rich source of candidate peptides and proteins with potential diverse tissue and cellular origins that may reflect important disease-related information.

Supra-additive growth inhibition by a celecoxib analogue and carboxyamido-triazole is primarily mediated through apoptosis.

Combination studies of celecoxib and chemotherapeutic agents suggest that combining cyclooxygenase-2 inhibitors with other agents may have supra-additive or synergistic effects on tumor growth inhibition. Carboxyamido-triazole (CAI), a voltage-independent calcium channel inhibitor, has been shown to induce growth inhibition and apoptosis in cancer cells. We found that continuous exposure to cytostatic doses of CAI and LM-1685, a celecoxib analogue, reduced the proliferation and survival of seven human cancer cell lines by at least one log (P < or = 0.001) over either agent alone. To explore the mechanism of action of this combination, we further studied the effects of LM-1685/CAI on CCL-250 colorectal carcinoma cells. We found that the supra-additive antiproliferative effects occurred throughout a range of LM-1685 doses (5-25 micromol/L) and paralleled a decrease in COX-2 activity as measured by prostaglandin E2 production. In these cells, treatment with LM-1685/CAI suppressed the extracellular signal-regulated kinase pathway within the first hour but ultimately results in high, sustained activation of ERK over a 9-day period (P = 0.0005). Suppression of cyclin D1 and phospho-AKT, and cleavage of caspase-3 and PARP were concomitant with persistent ERK activation. Addition of PD98059, a MEK-1 inhibitor, suppressed ERK activation and significantly but incompletely reversed these signaling events and apoptosis. Flow cytometry experiments revealed that the CAI/LM-1685 combination induced a 3-fold increase in apoptosis over control (P = 0.005) in 3 days. We show that the combination of CAI and LM-1685 produces a cytotoxic effect by suppressing proliferation and triggering apoptosis.

Pathology of the future: molecular profiling for targeted therapy.

Recent evidence suggests that each patient's cancer has a unique subset of molecular pathogenetic derangements. These derangements may both genetic and proteomic alterations. Genomic and proteomic research tools enable genome-wide assessment of gene expression as well as kinase driven cell signaling events. These tools are illuminating the molecular derangements of individual tumors, even if these tumors have similar morphological characteristics. A combination of laser capture microdissection with multiplexed phosphoproteomic analysis using reverse phase protein microarray technology is being used to identify protein molecular signatures of individual tumors. The in vivo state of multiple kinase driven signal pathways may be evaluated by reverse phase protein microarray with a panel of specific antibodies developed based upon our knowledge of biological processes. Molecular profiling of individual patient's tumors is currently being evaluated in clinical trials at the National Institutes of Health, National Cancer Institute for monitoring Epidermal Growth Factor (EGF) cell signaling events for patients with breast and ovarian cancer.

Importance of communication between producers and consumers of publicly available experimental data.

The application of mass spectrometry to discover new cancer biomarkers is in its infancy. Many of these new markers are low-abundance proteins that exist as fragments associated with carrier proteins. Although reproducibility is key to the use of mass spectrometry for ion fingerprint analysis, the scientific community has yet to establish a common platform or standardized operating procedures that are necessary for intra- and inter-laboratory comparison. In an effort to assist others who are perfecting mass spectrometry platforms for profiling, ongoing experimental data were posted for public consumption. An unintended consequence of unrestricted access to experimental data is the risk of inappropriate conclusions drawn and publicly disseminated that could have been avoided by communication between the producers and consumers of the data. Such disputes, however, should not divert us from the validation of this promising new approach.

Serum proteomics in cancer diagnosis and management.

Mass spectrometry-based diagnostics has the potential to revolutionize molecular medicine. Using modern mass-spectrometer technologies, clinical tests can be developed that are practical, robust, accurate, and inexpensive. Serum proteomic pattern profiling couples mass spectrometry with adaptive artificial-intelligence-based bioinformatics, which can now be employed to detect pathological states reflected in the serum proteome. With this approach, rapid and cost-effective tests with exquisite clinical sensitivity and specificity are emerging. These tools may dramatically change how disease is detected, monitored, and managed.

Protein microarrays: molecular profiling technologies for clinical specimens.

Proteomics, the study of protein function within biologic systems, will further our understanding of cancer pathogenesis. Coupled with transcript profiling, proteomics can herald the advent of molecular therapy tailored to the individual patient's neoplasm. Protein microarrays, one emerging class of proteomic technologies, have broad applications for discovery and quantitative analysis. This technology is uniquely suited to gather information about the post-translational modifications of proteins reflecting the activity state of signal pathways and networks. Protein microarrays now make it feasible to conduct signal network profiling within cellular samples. Nevertheless, to be successful, design and use of protein microarrays must take into consideration enormous analytical challenges. A subclass of protein microarrays, Reverse Phase Arrays, created to meet these challenges, has been optimized for use with tissue specimens, and is now in use for the analysis of biopsy samples for clinical trial research.

Protein microarrays: meeting analytical challenges for clinical applications.

Protein microarrays, one emerging class of proteomic technologies, have broad applications for discovery and quantitative analysis. A rapidly expanding use of this technology is the acquisition of information about the posttranslational modifications of proteins reflecting the activity state of signal pathways and networks, and is now employed for the analysis of biopsy samples in clinical trial research.

Biomarker amplification by serum carrier protein binding.

Mass spectroscopic analysis of the low molecular mass (LMM) range of the serum/plasma proteome is a rapidly emerging frontier for biomarker discovery. This study examined the proportion of LMM biomarkers, which are bound to circulating carrier proteins. Mass spectroscopic analysis of human serum following molecular mass fractionation, demonstrated that the majority of LMM biomarkers exist bound to carrier proteins. Moreover, the pattern of LMM biomarkers bound specifically to albumin is distinct from those bound to non-albumin carriers. Prominent SELDI-TOF ionic species (m/z 6631.7043) identified to correlate with the presence of ovarian cancer were amplified by albumin capture. Several insights emerged: a) Accumulation of LMM biomarkers on circulating carrier proteins greatly amplifies the total serum/plasma concentration of the measurable biomarker, b) The total serum/plasma biomarker concentration is largely determined by the carrier protein clearance rate, not the unbound biomarker clearance rate itself, and c) Examination of the LMM species bound to a specific carrier protein may contain important diagnostic information. These findings shift the focus of biomarker detection to the carrier protein and its biomarker content.