4-Nitro-7-piperazino-2,1,3-benzoxadiazole as a reagent for monitoring of airborne isocyanates by liquid chromatography

4-Nitro-7-piperazino-2,1,3-benzoxadiazole (NBDPZ) is presented as a new reagent for the determination of mono- and diisocyanates in air samples. NBDPZ readily reacts with the airborne analytes, thus yielding the corresponding urea derivatives, which are subsequently separated by means of reversed-phase liquid chromatography. On a phenyl-modified stationary phase, excellent baseline separation for numerous mono- and diisocyanate derivatives is obtained. Both diode array and fluorescence detection are performed with limits of detection of 11-35 and 5-9 nmol/L for the individual derivatives, respectively. In contrast to established derivatizing agents for the analysis of isocyanates, NBDPZ provides for increased selectivity due to the favorable detection wavelengths in the visible range (UV/visible, absorption maximums approximately 480 nm; fluorescence, excitation maximums approximately 470 nm, emission maximums approximately 535 nm). In addition, the high molar absorptivities of the reagent and the derivatives provide excellent sensitivity that is superior to most literature-known methods. Finally, air sampling methods comprising both the use of impingers and test tubes are developed and successfully applied to the determination of isocyanates in gaseous samples. Excellent recovery reaching values of >90% is observed for each of the two techniques investigated.     

An information-processing model of the decision to seek professional help.

Despite the presence of quality mental health care in many communities, people tend to avoid seeking help and wind up languishing in their problems unnecessarily. For the professional to better understand how to reach these individuals, an information-processing model is presented that examines the effects of people's interpretation of their environment and their symptoms on their decision to seek mental health services. Using the model as a guide, suggestions are presented for practitioners who wish to provide services to those who are in need of professional help, yet are hesitant to obtain it. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Concerns of the dry-cleaning industry: a qualitative investigation of labor and management

BACKGROUND: Occupational scientists agree there are hazards associated with dry-cleaning, but do dry-cleaning owners and workers concur? Knowledge of owners' and workers' perceptions can help guide intervention efforts to reduce worker exposure. To better understand these issues, a qualitative study was conducted using focus group methodology and constant comparative analysis. METHODS: Two owner and four worker focus groups were held. RESULTS: Findings suggest that overall, health and safety issues were not of great concern. Owners were primarily concerned with the economic impact of regulations. Workers did express some anxiety about solvent exposure and burns, but most felt that these hazards were "just part of the job." Also, other than the installation of air-conditioning in the shops and the provision of health benefits, workers could not think of ways health and safety on the job could be improved. CONCLUSIONS: These findings will be used to develop comprehensive safety and health interventions (e.g., engineering plus education and training) in dry-cleaning shops.     

Blood-brain barrier carrier-mediated transport and brain metabolism of amino acids

We have examined the effects of the macrocyclic lactone protein kinase C (PKC) activator bryostatin 1 on taxol-induced apoptosis and inhibition of clonogenicity in the human monocytic leukemia cell line U937. Exposure of cells to bryostatin 1 (10 nM; 15 hr) after (but not before) a 6-hr incubation with 0.5 microM taxol significantly increased apoptosis and resulted in an approximately 3 log reduction in clonogenicity. Cell cycle analysis revealed that the increase in apoptotic cells following bryostatin 1 treatment occurred primarily in the population undergoing taxol-mediated G2M arrest. The actions of bryostatin 1 were not attributable to potentiation of taxol-induced tubulin stabilization or to a reduction in the intracellular retention of taxol. Following exposure of cells to taxol, the Bcl-2 protein displayed an alteration in mobility that was not modified appreciably by bryostatin 1 treatment. The mobility shift in Bcl-2 protein from cells exposed to taxol followed by bryostatin 1 was eliminated by treatment of lysates with the protein phosphatase 2A (PP2A); the latter effect was blocked by okadaic acid. Treatment of cells with taxol followed by bryostatin 1 did not increase the amount of total Bax (compared with treatment with taxol alone), but did increase the amount of free Bax in the supernatant fraction. Finally, the ability of bryostatin 1 to potentiate taxol-induced apoptosis in U937 cells was mimicked closely by 2'-amino-3'-methoxyflavone (PD98059), a specific inhibitor of the mitogen-activated protein kinase (MAPK) kinase (MEK). Collectively, these findings indicate that bryostatin 1 increases the susceptibility of U937 cells to taxol-induced apoptosis and inhibition of clonogenicity. They also raise the possibility that this phenomenon may involve functional alterations in Bcl-2 and/or other proteins involved in regulation of the cell death pathway.     

Altered release of prostaglandins by opioids contributes to impaired cerebral hemodynamics following brain injury

OBJECTIVES: After fluid percussion brain injury (FPI) in the newborn pig, pial arteries constrict and responses to dilator stimuli, including opioids, are blunted. This study was designed to determine if altered release of prostaglandins contributes to blunted opioid dilation of cerebral arteries in newborn piglets following brain injury. DESIGN: Prospective, in vivo, cerebral hemodynamic animal study. SETTING: University research laboratory. SUBJECTS: Newborn (1- to 5-days old) piglets of either gender. INTERVENTIONS: In anesthetized, newborn, 1- to 5-day-old pigs, a closed cranial window was used to measure pial artery diameter and to collect cortical periarachnoid cerebrospinal fluid (CSF) for determination of 6-keto-PGF1alpha, the stable metabolite of prostaglandin I2 (PGI2) and thromboxane B2 (TXB2), the stable metabolite of TXA2, via radioimmunoassay. FPI of moderate severity (1.9 to 2.3 atmospheres) was produced by using a pendulum to strike a piston on a saline-filled cylinder that was fluid coupled to the brain via a hollow screw inserted through the cranium. MEASUREMENTS AND MAIN RESULTS: Methionine enkephalin (Met) vasodilation was blunted after FPI but was partially restored with indomethacin pretreatment (5 mg/kg i.v.) (8 +/- 1 [SEM] %, 13 +/- 1%, and 20 +/- 1% vs. 1 +/- 1%, 3 +/- 1%, and 5 +/- 1% vs. 7 +/- 1%, 10 +/- 1%, and 15 +/- 1%, respectively, for 10(-10), 10(-8), and 10(-6) M Met during control conditions, after FPI, and after FPI pretreated with indomethacin, n = 6). Similarly, restoration of Met dilation after FPI was observed with SQ 29,548, a TXA2 antagonist. Met-induced 6-keto-PGF1alpha release was blunted following FPI (889 +/- 20, 1130 +/- 33, and 1886 +/- 59 vs. 2630 +/- 36, 2775 +/- 30, and 2825 +/- 36 pg/mL for control, 10(-10), and 10(-6) M Met before and after FPI, respectively, n = 6). In contrast, Met-induced TXB2 release was enhanced after FPI (340 +/- 20, 423 +/- 25, and 473 +/- 30 pg/mL vs. 518 +/- 30, 726 +/- 90, and 901 +/- 35 pg/mL for control, 10(-10), and 10(-6) M Met before and after FPI, respectively, n = 6). Leucine enkephalin- and dynorphin-induced dilation and associated prostaglandin release were similarly altered following FPI. Beta endorphin-induced constriction was enhanced following FPI, and these potentiated responses were blunted after indomethacin or SQ 29,548 pretreatment. CONCLUSIONS: These data show that FPI increases CSF 6-keto-PGF1alpha and TXB2 concentrations. These data suggest that altered release of prostaglandins by opioids contribute to impaired cerebral hemodynamics following FPI in piglets.     

Double free-flap reconstruction of massive defects involving the lip, chin, and mandible

Men develop perioperative ulnar neuropathies more frequently than women. To determine the role of anatomical gender differences in the development of these neuropathies, we performed several studies of the anatomy of the ulnar nerve, cubital tunnel, and elbow region. These studies included detailed dissection of male and female embalmed and unembalmed cadavers, ultrasound measurements of the tissue layers at the elbow, and measurement of various dimensions of the coronoid process of the ulna in multiple skeletal sets. No gross anatomical differences were found between genders regarding the course of the ulnar nerve through the upper limb. However, there was a strikingly larger (2-19 times greater) fat content on the medial aspect of the elbow in women compared to men, and the tubercle of the coronoid process was approximately 1.5 times larger in men (P < or = .002, rank sum test). Our finding suggest that the tubercle of the coronoid process is a likely area for external compression-induced ischemia of the ulnar nerve because the nerve and its arterial supply (the posterior ulnar recurrent artery) are covered at the tubercle only by skin, subcutaneous fat, and a very thin aponeurosis of the flexor carpi ulnaris. Importantly, this tubercle is larger and the nerve and blood vessels passing by it are less protected by subcutaneous fat in men than in women. These two anatomical differences between men and women may contribute to the increased frequency of perioperative ulnar neuropathy induced by external pressure at the medial aspect of the elbow in men.     

Involvement of CD14 and complement receptors CR3 and CR4 in nuclear factor-kappaB activation and TNF production induced by lipopolysaccharide and group B streptococcal cell walls

This study was undertaken to evaluate the role of CD14 and complement receptors type 3 (CR3) and 4 (CR4) in mediating TNF release and NF-kappaB activation induced by LPS and cell wall preparations from group B streptococci type III (GBS). LPS and GBS caused TNF secretion from human monocytes in a CD14-dependent manner, and soluble CD14, LPS binding protein, or their combination potentiated both LPS- and GBS-induced activities. Blocking of either CD14 or CD18, the common beta-subunit of CR3 and CR4, decreased GBS-induced TNF release, while LPS-mediated TNF production was inhibited by anti-CD14 mAb only. Chinese hamster ovary cell transfectants (CHO) that express human CD14 (CHO/CD14) responded to both LPS and GBS with NF-kappaB translocation, which was inhibited by anti-CD14 mAb and enhanced by LPS binding protein. While LPS showed fast kinetics of NF-kappaB activation in CHO/CD14 cells, a slower NF-kappaB response was induced by GBS. LPS also activated NF-kappaB in CHO cells transfected with either human CR3 or CR4 cDNA, although responses were delayed and weaker than those of CHO/CD14 cells. In contrast to LPS, GBS failed to induce NF-kappaB in CHO/CR3 or CHO/CR4 cells. Both C3H/OuJ (Lps[n]) and C3H/HeJ (Lps[d]) mouse peritoneal macrophages responded to GBS with TNF production and NF-kappaB translocation, whereas LPS was active only in C3H/OuJ macrophages. Thus, LPS and GBS differentially involve CD14 and CR3 or CR4 for signaling NF-kappaB activation in CHO cells and TNF release in human monocytes, and engage a different set of receptors and/or intracellular signaling pathways in mouse macrophages.     

Hepatotoxicity of anticholesterol, cardiovascular, and endocrine drugs and hormonal agents

Drugs in these categories may have effects on several organs in addition to the liver. For example, amiodarone may produce thyroid and corneal injury apart from or in addition to the phospholipidosis seen in the liver. Oral contraceptive steroids remain a rare but important concern for developing hepatic adenomas and possibly hepatocellular carcinoma, as well as a risk factor for developing Budd-Chiari syndrome in long-term users. Among the antihyperlipidemic agents, nicotinic acid, especially the sustained release formulations, may produce severe of even fatal hepatic injury. Increasing numbers of reports of hepatotoxicity from newer beta blockers and angiotensin-converting enzyme inhibitors require ongoing vigilance in patients receiving these medications.