Haematological and histological changes in fish Heteropneustes fossilis exposed to pesticides from industrial waste water

The present study investigated the potential changes in hematologic parameters and histology of fish Heteropneustes fossilis when exposed to industrial waste water of different concentrations. The toxicant enter into the fish body from different rout, inhalation, dermal oral, and other several rout for entering in the fish body. The blood parameters of fish H. fossilis control group and treatment were investigated on 1st, 5th, 10th, and 20th days of experiment, hematologic variation was observed in RBC, WBC, MCV, MCH, and MCHC count. Histopathologic changes in liver, intestine, gill, muscle, and heart showed increasing degrees of damage in the tissues in correlation with the accumulation pattern of pesticides, while liver, intestine, gill, muscle, and heart of control group exhibited a normal architecture. Toxic effects of pesticides vary in different organs of the fish H. fossilis significant. The fish exposed to higher concentration showed uncoordinated alterations in behavioral responses, especially erratic and jerky swimming, physiologic, malformation, histologic, hematologic and biochemical changes, frequent surfacing and in gulping, mucus secretion, an increase in opercular movement, and copious secretion of mucus of all over the body.     

Disruption of the somitic molecular clock causes abnormal vertebral segmentation

Somites are the precursors of the vertebral column. They segment from the presomitic mesoderm (PSM) that is caudally located and newly generated from the tailbud. Somites form in synchrony on either side of the embryonic midline in a reiterative manner. A molecular clock that operates in the PSM drives this reiterative process. Genetic manipulation in mouse, chick and zebrafish has revealed that the molecular clock controls the activity of the Notch and WNT signaling pathways in the PSM. Disruption of the molecular clock impacts on somite formation causing abnormal vertebral segmentation (AVS). A number of dysmorphic syndromes manifest AVS defects. Interaction between developmental biologists and clinicians has lead to groundbreaking research in this area with the identification that spondylocostal dysostosis (SCD) is caused by mutation in Delta-like 3 (DLL3), Mesoderm posterior 2 (MESP2), and Lunatic fringe (LFNG); three genes that are components of the Notch signaling pathway. This review describes our current understanding of the somitic molecular clock and highlights how key findings in developmental biology can impact on clinical practice.     

Cryptococcal phospholipase B antigen is not detected in serum of patients infected with Cryptococcus neoformans using a sandwich enzyme-linked immunosorbent assay

Extracellular phospholipase B (PLB) is a virulence determinant of Cryptococcus neoformans and Cryptococcus gattii. In this study, we developed a sensitive enzyme-linked immunosorbent assay (ELISA) for PLB antigen with a detection limit of 3.9 ng mL(-1). PLB was detected in culture supernatants of C. neoformans and C. gattii. PLB, however, was not detected in sera of seven human patients and 10 feline patients with active cryptococcosis. Furthermore, none of five rats with extensive pulmonary C. gattii infection had a positive ELISA test result. In conclusion, cryptococcal PLB could not be detected in serum using a PLB antigen-based ELISA. Despite its sensitivity, this ELISA is of limited diagnostic value. Exploration of further extracellular molecules suitable for serodiagnosis of active cryptococcal infection is warranted.     

Two new protease-inhibiting glycosphingolipids from Buddleja crispa

Crispins A (1) and B (2), two new glycosphingolipids, were isolated from the whole plant Buddleja crispa, along with three known compounds: alpha-amyrin, linoleic acid, and stigmasterol. Their structures were elucidated by chemical and spectroscopic techniques. Both 1 and 2 showed significant inhibitory activity against alpha-chymotrypsin in a concentration-dependent manner.     

Mating system and inbreeding depression in whitebark pine (Pinus albicaulis Engelm.)

Mating system and inbreeding depression in quantitative traits of whitebark pine (Pinus albicaulis Engelm.) was determined using isozymes and a seedling common garden experiment. Simultaneous isozyme analysis of embryo and haploid megagametophyes from progeny arrays of families in three distinct geographic regions (Oregon, Montana, and southern British Columbia) was used to estimate parental and progeny inbreeding coefficients, as well as regional and family mean multilocus outcrossing rates (t _m). Quantitative trait family means of seedlings from the same families growing in two temperature treatments in a common garden experiment were regressed on the estimated inbreeding coefficient to determine the presence and magnitude of inbreeding depression. Regional estimates of t _m ranged from 0.73 to 0.93, with a mean over all regions of 0.86. Family mean t _m values indicated predominant outcrossing; however, some individuals experienced substantial inbreeding. The Oregon region had a significant excess of heterozygotes in the parental generation relative to Hardy–Weinberg equilibrium, while both the Oregon and southern BC regions had a heterozygote deficiency in progeny, suggesting selection against inbred individuals. Biomass in the ambient temperature treatment for the southern BC region was the only trait significantly related to inbreeding coefficient. The mean inbreeding coefficient for this region was 0.25, and based on this relationship, mean predicted biomass would be reduced by 19.6% in this region if inbred individuals are not removed by selection. The estimated outcrossing rate of whitebark pine is slightly lower than most wind-pollinated conifers, and while most individuals are highly outcrossing, some experience substantial inbreeding.     

Isolation and enzyme-inhibition studies of the chemical constituents from Ajuga bracteosa

Bractin A (=(2S,3S,4R,5E)-2-{[(2R)-2-hydroxydodecanoyl]amino}triacont-5-ene-1,3,4-triol; 1) and bractin B (=(2S,3S,4R,5E,8E)-2-{[(2R)-2-hydroxyhexacosanoyl]amino}pentadeca-5,8-diene-3,4,15-triol 1-O-beta-D-glucopyranoside; 2), new sphingolipids, and bractic acid (=(5Z,10Z,15Z)-2-decyl-4,7,8,12,13,17,18-heptahydroxy-20,23-dioxopentacosa-5,10,15-trienoic acid; 3), a long-chain polyhydroxy acid, were isolated from the whole plant Ajuga bracteosa along with four known diterpenoids 4-7. Their structures were deduced by spectral studies including 1D- and 2D-NMR spectroscopy. Compounds 1-3 displayed inhibitory potential against enzyme lipoxygenase, while compounds 4-7 inhibited cholinesterase enzymes in a concentration-dependent manner with IC(50) values in the range 10.0-33.0, 14.0-35.2, and 10.0-19.0 microM for lipoxygenase, acetylcholinesterase, and butyrylcholinesterase, respectively. Lineweaver-Burk, and Dixon plots, and their secondary replots indicated that all compounds exhibit non-competitive type of inhibition with K(i) values in the range of 9.5-35.2, 15.2-36.0, and 11.6-20.5 microM, for lipoxygenase, acetylcholinesterase, and butyrylcholinesterase, respectively.     

Modelling an outbreak of an emerging pathogen

To illustrate the usefulness of mathematical models to the microbiology and medical communities, we explain how to construct and apply a simple transmission model of an emerging pathogen. We chose to model, as a case study, a large (>8,000 reported cases) on-going outbreak of community-acquired meticillin-resistant Staphylococcus aureus (CA-MRSA) in the Los Angeles County Jail. A major risk factor for CA-MRSA infection is incarceration. Here, we show how to design a within-jail transmission model of CA-MRSA, parameterize the model and reconstruct the outbreak. The model is then used to assess the severity of the outbreak, predict the epidemiological consequences of a catastrophic outbreak and design effective interventions for outbreak control.     

Alstrom syndrome (OMIM 203800): a case report and literature review

Hereditary chronic pancreatitis (HCP) is a very rare form of early onset chronic pancreatitis. With the exception of the young age at diagnosis and a slower progression, the clinical course, morphological features and laboratory findings of HCP do not differ from those of patients with alcoholic chronic pancreatitis. As well, diagnostic criteria and treatment of HCP resemble that of chronic pancreatitis of other causes. The clinical presentation is highly variable and includes chronic abdominal pain, impairment of endocrine and exocrine pancreatic function, nausea and vomiting, maldigestion, diabetes, pseudocysts, bile duct and duodenal obstruction, and rarely pancreatic cancer. Fortunately, most patients have a mild disease. Mutations in the PRSS1 gene, encoding cationic trypsinogen, play a causative role in chronic pancreatitis. It has been shown that the PRSS1 mutations increase autocatalytic conversion of trypsinogen to active trypsin, and thus probably cause premature, intrapancreatic trypsinogen activation disturbing the intrapancreatic balance of proteases and their inhibitors. Other genes, such as the anionic trypsinogen (PRSS2), the serine protease inhibitor, Kazal type 1 (SPINK1) and the cystic fibrosis transmembrane conductance regulator (CFTR) have been found to be associated with chronic pancreatitis (idiopathic and hereditary) as well. Genetic testing should only be performed in carefully selected patients by direct DNA sequencing and antenatal diagnosis should not be encouraged. Treatment focuses on enzyme and nutritional supplementation, pain management, pancreatic diabetes, and local organ complications, such as pseudocysts, bile duct or duodenal obstruction. The disease course and prognosis of patients with HCP is unpredictable. Pancreatic cancer risk is elevated. Therefore, HCP patients should strongly avoid environmental risk factors for pancreatic cancer.