Effect of biosolids amendment on the fate and mobility of non-steroidal anti-inflammatory drugs (NSAIDs) in a field-based lysimeter cell study.

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used globally to treat and prevent illness. Biosolids change physico-chemical characteristics of soil and can affect the mobility of NSAIDs. A field-based lysimeter study evaluated the effect of three rates (0, 7, and 28 Mg ha-1) of alkaline treated biosolids (ATB) on the leaching potential of naproxen (NPX), ibuprofen (IBF), and ketoprofen (KTF) over 34 days in a sandy loam textured soil. Although all three NSAIDs in the lysimeter cells vertically migrated to deeper soil depths after spiking, the sum of all NPX, IBF, and KTF detected in the leachate samples from all treatments were only 0.03%, 0.02%, and 0.04% of the initial spiking mass to the surface soil, respectively. A mass balance analysis indicated a low accumulation of these compounds in the soil at the end of the study (Day 34) from all treatments with only 4.8%, 0.5%, and 0.7% of initial spiked NPX, IBF, and KTF, respectively. Application of ATB significantly increased soil pH and organic matter (OM) content of the soils but did not impact retention of the compounds in the soil profile. Overall, all three NSAIDs in the present study presented low mobility in the loamy sand textured agricultural soil.

Examining the ultraviolet optical screening tool as a viable means for delineating a contaminated organic sediment.

Rapid and accurate delineation of contaminated sediments in marine environments is critical for the effective assessment of site risks and the development of appropriate remedial action plans. In this study, a new application of the ultraviolet optical screening tool (UVOST) equipped with electrical conductivity measurement (UVOST-EC) is proposed to delineate a water-covered sediment contaminated with dioxins and furans in a decommissioned pulp and paper wastewater stabilization basin. Bench scale experiments are presented that were used to develop a UVOST-EC interpretation method for delineating between two different sediment types present in the basin: an anthropogenically derived organic rich contaminated sediment ("black sediment") and a naturally occurring grey organic silt sediment with marine provenance ("grey sediment"). The method involves comparative analysis of fluorescence and electrical conductivity signatures between the two sediments. Results indicate that each sediment type presents unique "signatures" related to fluorescence and electrical signals which corresponds to variability in their physio-chemical structure. Almost 100 UVOST-EC tests performed at the study site were paired with ex situ physical gravity core measurements of the black sediment to test the accuracy of the UVOST-EC-based method. A statistical analysis at seven sample "cluster" sites (i.e. multiple sub-samples within a defined area) indicated that the mean of sediment thickness obtained by the UVOST-EC measurement technique at a given site were not significantly different (p = 0.05) from measurements derived from sediment gravity core measurements. The UVOST-EC-based sediment thickness delineation method reliably determined the thickness of the dioxin and furan contaminated sediments as compared to gravity core determination for the sediment in this study. Application of this approach to other studies should be assessed in a similar manner. The UVOST-EC method offers health and safety, cost, logistics, and data interpretation benefits.

Biodegradation kinetics of individual and mixture non-steroidal anti-inflammatory drugs in an agricultural soil receiving alkaline treated biosolids.

Land application of biosolids is one potential source of pharmaceuticals and personal care products (PPCPs) into agricultural soils. Degradation is an important natural attenuation pathway that affects the fate and transport of PPCPs in the soil system and biosolids application could alter the process. The present study assessed the effect of individual and mixture compound environments on the biodegradation rate and half-life of three non-steroidal anti-inflammatory drugs (NSAIDs), naproxen (NPX), ibuprofen (IBF), and ketoprofen (KTF), in a loamy sand textured agricultural soil receiving an alkaline treated biosolid (ATB) amendment. A prolonged half-life of the target NSAIDs was determined for sterile soils and shorter half-lives in unsterile soils, indicating the loss of target compounds in all treatments was mainly attributed to biodegradation and followed first-order kinetics. IBF and NPX showed low to moderate persistence in soil and ATB amended soil, with half-lives ranging from 4.9 to 14.8 days, while KTF appeared to be highly persistent with an average half-life of 33 days. The order in which the target NSAIDs disappeared in both soil and ATB amended soil was: IBF > NPX > KTF, for both individual and mixture compound treatments. Soils that received the ATB amendment demonstrated inhibited degradation of NPX in all treatments, as well as IBF and KTF in individual compound treatment over the 14-day incubation study. We also observed an inhibition effect from the ATB amendment in sterile soil treatments. In mixture compound treatments, IBF degradation was inhibited in both soil and ATB amended soil. The degradation rate of KTF in mixture compound environment in soil was lower, while the opposite effects were observed in ATB amended soils. For NPX, the degradation was enhanced in mixture compound environment in ATB amended soil, while the same degradation rate of NPX was calculated in soil.

Failure of neuraxial anaesthesia in a patient with Velocardiofacial syndrome.

Velocardiofacial or 22q11 deletion syndrome is a genetic condition caused by deletion 22q11, the deletion of a small segment of the long arm of chromosome 22. To our knowledge this is the first case report of a woman with Velocardiofacial syndrome presenting in late pregnancy for caesarean delivery. She had undergone a Tetralogy of Fallot repair as an infant and had residual pulmonary regurgitation. In addition examination revealed micrognathia and scoliosis. Neuraxial anaesthesia was unsuccessful and subsequent conversion to general anaesthesia was necessary despite concerns regarding her facial abnormalities, pulmonary regurgitation and mild intellectual impairment.

Physicochemical characterization of cement kiln dust for potential reuse in acidic wastewater treatment.

Cement kiln dust (CKD) is a fine-grained material produced during the manufacture of cement. Current reuse options are limited and the bulk of CKD not reused in the cement manufacturing process is sent to landfills or stored on-site. Due to the calcium oxide (CaO) content of CKD, it has the potential to be used as a replacement for lime in treating acidic wastewaters such as acid rock drainage (ARD). This paper outlines the results of an examination of the physical and chemical properties of CKD samples collected from six cement plants. The CKD samples were analyzed for major oxides using X-ray diffraction (XRD), available lime, specific surface area, particle size, and morphology using scanning electron microscope (SEM) and compared with a commercial quicklime product. Conductivity, pH, and calcium concentrations of slaked CKD and quicklime solutions were used as indicators of reactivity of the CKD. Slaking of two of the CKD samples with the highest free lime contents (e.g., 34 and 37% free CaO) gave elevated pH values statistically comparable to those of the commercial quicklime sample that was characterized as having 87% available CaO. Acid neutralization trials indicate that even CKD samples with low free lime contents could be effective at neutralizing acidic wastewaters.

Adsorption, sedimentation, and inactivation of E. coli within wastewater treatment wetlands.

Bacteria fate and transport within constructed wetlands must be understood if engineered wetlands are to become a reliable form of wastewater treatment. This study investigated the relative importance of microbial treatment mechanisms in constructed wetlands treating both domestic and agricultural wastewater. Escherichia coli (E. coli) inactivation, adsorption, and settling rates were measured in the lab within two types of wastewater (dairy wastewater lagoon effluent and domestic septic tank effluent). In situ E. coli inactivation was also measured within a domestic wastewater treatment wetland and the adsorption of E. coli was also measured within the wetland effluent. Inactivation of E. coli appears to be the most significant contributor to E. coli removal within the wastewaters and wetland environments examined in this study. E. coli survived longer within the dairy wastewater (DW) compared to the domestic wastewater treatment wetland water (WW). First order rate constants for E. coli inactivation within the WW in the lab ranged from 0.09 day(-1) (d(-1)) at 7.6 degrees C to 0.18d(-1) at 22.8 degrees C. The average in situ rate constant observed within the domestic wetland ranged from 0.02 d(-1) to 0.03 d(-1) at an average water temperature of 17 degrees C. First order rate constants for E. coli inactivation within the DW ranged from 0.01 d(-1) at 7.7 degrees C to 0.04 d(-1) at 24.6 degrees C. Calculated distribution coefficients (K(d)) were 19,000 mL g(-1), 324,000 mL g(-1), and 293 mL g(-1) for E. coli with domestic septic tank effluent (STE), treated wetland effluent (WLE), and DW, respectively. Approximately 50%, 20%, and 90% of E. coli were "free floating" or associated with particles <5 microm in size within the STE, WLE, and DW respectively. Although 10-50% of E. coli were found to associate with particles >5 microm within both the STE and DW, settling did not appear to contribute to E. coli removal within sedimentation experiments, indicating that the particles the bacteria were associated with had very small settling velocities. The results of this study highlight the importance of wastewater characterization when designing a treatment wetland system for bacterial removal. This study illustrated the level of variability in E. coli removal processes that can be observed within different wastewater, and wetland environments.

How academic psychiatry can better prepare students for their future patients. Part I: the failure to recognize depression and risk for suicide in primary care; problem identification, responsibility, and solutions.

The author, after a review of the relevant literature, found that depression and the risk for suicide remain unacceptably underrecognized in primary care (PC). The negative consequences are substantial for patients and their physicians. Suicide prevention in PC begins with the recognition of depression because suicide occurs largely during depression. In this article (Part I), the author suggests causes, responsibilities, and solutions for that failure. He also addresses the role of academic psychiatry's traditional curriculum. The comprehensive, initial diagnostic interview that is typically taught to medical students in psychiatry may decrease recognition in PC care because of the time required to complete it. In Part II, the author offers guidelines to develop a weekly interview course with an instrument targeting abbreviated diagnostic screening for only the most critical psychiatric problems such as depression and the risk for suicide.

How academic psychiatry can better prepare students for their future patients. Part II: a course in ultra-brief initial diagnostic screening suitable for future primary care physicians.

Depression is inadequately treated in primary care (PC), primarily because of a failure to recognize symptoms of depression. The results can be catastrophic and include death by suicide. The prevention of suicide is a critical function of physicians. The recognition of depression is the first step to preventing suicide because suicide predominately occurs during depression. The traditional, comprehensive psychiatric interview typically taught by academic psychiatry may inhibit recognition in PC settings because it takes too much time. Attempts to integrate a brief psychiatric interview into the PC-patient interaction to meet these needs of increasing recognition have had mixed results. Instruction to medical students on psychiatry in the use of an ultra-brief screening instrument for these disorders, suitable for the time-pressured PC environment, could help attain the goal of improved recognition. A Four-Question, 90-Second Depression Screen is described and recommended. The author offers a detailed format for establishing an interview course to impart such skills that is appropriate for students and residents in their psychiatry or PC rotations.

Disorders of thought are severe mood disorders: the selective attention defect in mania challenges the Kraepelinian dichotomy a review.

Kraepelin said severe mental illness was due to 2 diseases subsequently characterized as disorders of thought vs disorders of mood, ie, the Kraepelinian dichotomy. Schizophrenia, traditionally considered the disorder of thought, has been defined by the presence of hallucinations, delusions, catatonia, and disorganization. Tangentiality, derailment, loose associations, and thought blocking are typically considered pathognomonic of schizophrenia. By contrast, the mood disorders have been characterized only as disorders of the emotions, though both depression and mania, when severe, are now recognized to include the same psychotic features traditionally considered diagnostic of schizophrenia. This article addresses disordered thinking in mania in order to clarify the relationship between schizophrenia and psychotic mood disorders. Normally, the brain's selective attention mechanism filters and prioritizes incoming stimuli by excluding from consciousness extraneous, low-priority stimuli and grading the importance of more relevant data. Because this "filter/prioritizer" becomes defective in mania, tangential stimuli are processed without appropriate prioritization. Observed as distractibility, this symptom is an index of the breakdown in selective attention and the severity of mania, accounting for the signs and symptoms of psychotic thinking. The zone of rarity between schizophrenia and psychotic mood disorders is blurred because severe disorders of mood are also disorders of thought. This relationship calls into question the tenet that schizophrenia is a disease separate from psychotic mood disorders. Patients whose case histories are discussed herein gave their written informed consent to participate in this institutional human subjects committee-approved protocol.

The schizophrenias, the neuroses and the covered wagon; a critical review.

OBJECTIVE: In order to compare their validity, this review applies scientific standards for sustaining the neuroses, the schizophrenias and bipolar disorders as separate "bona-fide" psychiatric diseases. The standards for disease validation demand specific and unique symptoms. METHOD: We review a wide variety of clinical and basic science comparisons between schizophrenia and psychotic bipolar in a select English-language literature. RESULTS: Like covered wagons, the neuroses once served us well but became obsolete and were discarded or reorganized based on what was known about commonalities of symptoms, causation and pharmacological responsivity. Bipolar patients meet unique and specific diagnostic criteria and demonstrate consistent results across a variety of scientific disciplines. Neither the neuroses nor the schizophrenias have such unique or disease specific diagnostic criteria. Psychotic mood disorders account for the DSM diagnostic criteria for schizophrenia. A recent, selected but diverse basic science literature demonstrates surprising similarities between schizophrenia and psychotic bipolar which should not exist if these disorders are distinct. CONCLUSIONS: Like the neuroses, there is stigma, confusion and misunderstanding about the condition called schizophrenia, resulting in substantial negative impact on bipolar patients misdiagnosed as having schizophrenia. The psychoses, including the schizophrenias, likely are explained by a single disease, psychotic bipolar disorder, that has demonstrated a wide spectrum of severity of symptoms and chronicity of course, not traditionally recognized.

Schizoaffective disorders are psychotic mood disorders; there are no schizoaffective disorders.

Schizoaffective disorder (SA D/O), introduced in 1933 by Dr. Jacob Kasanin, represented a first, modest change in our concept about the diagnoses of psychotic patients away from the beliefs of E. Bleuler, i.e., that hallucinations and delusions define schizophrenia, and toward the recognition of a significant role for mood disorders. SA D/O established a connection between schizophrenia and mood disorders, traditionally considered mutually exclusive, a connection that has strengthened progressively toward the diagnostic unity of all three disorders. A basic tenet of medicine holds that if discrepant symptoms can be explained by one disease instead of two or more, it is likely there is only one disease. The scientific justification for SA D/O and schizophrenia as disorders distinct from a psychotic mood disorder has been questioned. The "schizo" prefix in SA D/O rests upon the presumption that the diagnostic symptoms for schizophrenia are disease specific. They are not, since patients with severe mood disorders can evince any or all of the "schizophrenic" symptoms. "Schizophrenic" symptoms mean "psychotic" and not any specific disease. These data and a very low interrater reliability for SA D/O suggest that the concepts of SA D/O and schizophrenia as valid diagnoses are flawed. Clinically SA D/O remains popular because it encompasses both schizophrenia and psychotic mood disorder when there is a diagnostic question. We present a review of the literature in table form based on an assignment of each article assigned to one of five categories that describe the possible relationships between SA D/O, schizophrenia and psychotic mood disorders. We conclude that the data overall are compatible with the hypothesis that a single disease, a mood disorder, with a broad spectrum of severity, rather than three different disorders, accounts for the functional psychoses.

Epstein-Barr virus that lacks glycoprotein gN is impaired in assembly and infection.

The Epstein-Barr virus (EBV) glycoproteins N and M (gN and gM) are encoded by the BLRF1 and BBRF3 genes. To examine the function of the EBV gN-gM complex, recombinant virus was constructed in which the BLRF1 gene was interrupted with a neomycin resistance cassette. Recombinant virus lacked not only gN but also detectable gM. A significant proportion of the recombinant virus capsids remained associated with condensed chromatin in the nucleus of virus-producing cells, and cytoplasmic vesicles containing enveloped virus were scarce. Virus egress was impaired, and sedimentation analysis revealed that the majority of the virus that was released lacked a complete envelope. The small amount of virus that could bind to cells was also impaired in infectivity at a step following fusion. These data are consistent with the hypothesis that the predicted 78-amino-acid cytoplasmic tail of gM, which is highly charged and rich in prolines, interacts with the virion tegument. It is proposed that this interaction is important both for association of capsids with cell membrane to assemble and release enveloped particles and for dissociation of the capsid from the membrane of the newly infected cell on its way to the cell nucleus. The phenotype of EBV lacking the gN-gM complex is more striking than that of most alphaherpesviruses lacking the same complex but resembles in many respects the phenotype of pseudorabies virus lacking glycoproteins gM, gE, and gI. Since EBV does not encode homologs for gE and gI, this suggests that functions that may have some redundancy in alphaherpesviruses have been concentrated in fewer proteins in EBV.

Epstein-Barr virus gH is essential for penetration of B cells but also plays a role in attachment of virus to epithelial cells.

Entry of Epstein-Barr virus (EBV) into B cells is initiated by attachment of glycoprotein gp350 to the complement receptor type 2 (CR2). A complex of three glycoproteins, gH, gL, and gp42, is subsequently required for penetration. Gp42 binds to HLA class II, which functions as an entry mediator or coreceptor and, by analogy with other herpesviruses, gH is then thought to be involved virus-cell fusion. However, entry of virus into epithelial cells is thought to be different. It can be initiated by attachment by an unknown glycoprotein in the absence of CR2. There is no interaction between gp42 and HLA class II and instead a distinct complex of only the two glycoproteins gH and gL interacts with a novel entry mediator. Again, by analogy with other viruses gH is thought to be critical to fusion. To investigate further the different roles of gH in infection of the two cell types and to examine its influence on the assembly of the gH-gL-gp42 complex, we constructed two viruses, one in which the gH open reading frame was interrupted by a cassette expressing a neomycin resistance gene and the gene for green fluorescent protein and one as a control in which the neighboring nonessential thymidine kinase gene was interrupted with the same cassette. Virus lacking gH exited from cells normally, although loss of gH resulted in rapid turnover of gL and gp42 as well. The virus bound normally to B lymphocytes but could not infect them unless cells and bound virus were treated with polyethylene glycol to induce fusion. In contrast, virus that lacked the gH complex was impaired in attachment to epithelial cells and the effects of monoclonal antibodies to gH implied that this resulted from loss of gH rather than other members of the complex. These results suggest a role for gH in both attachment and penetration into epithelial cells.

The use of thrombus precursor protein, D-dimer, prothrombin fragment 1.2, and thrombin antithrombin in the exclusion of proximal deep vein thrombosis and pulmonary embolism.

We examined various nonSTAT commercially available coagulation activation markers in an attempt to help diagnose or exclude the often subtle clinical presentations of proximal deep vein thrombosis (PDVT) and pulmonary embolism (PE). Fifty-five patients presenting to the Emergency Department were completely assessed. Eleven patients were diagnosed with PDVT, six patients were diagnosed with PE, and three patients were diagnosed with both PDVT and PE. Thrombus precursor protein (TpP) excluded the diagnosis in 19 of the 35 patients negative for PDVT and/or PE, D-Dimer in 15 patients, prothrombin fragment 1.2 in 17 patients, and thrombin-antithrombin (TAT) in 14 patients. Both the TpP and TAT enzyme-linked immunosorbent assay (ELISA) tests had 100% sensitivity and negative predictive value for evaluating PDVT and/or PE. The TpP ELISA had the highest specificity (54%) of all four markers studied.