Evaluation of workers exposed to elemental mercury using quantitative tests of tremor and neuromuscular functions

Workers exposed to metallic mercury vapor were subjects for tremor, EMG, and psychomotor tests. Regression analysis revealed statistically significant trends in these test results related to workers' urine mercury histories. Effects were subclinical, functionally insignificant and most associated with those workers whose urine mercury had exceeded 0.5 mg/L in the previous year. In agreement with previous reports, effects were reversible upon reduction of mercury exposure.     

Impaired release of natural killer cytotoxic factor(s) by peripheral blood lymphocytes in patients with chronic LGL-proliferative disease

BACKGROUND: Chronic LGL-proliferative disease (LGL-PD) is a clonal expansion of cells with large granular lymphocyte (LGL) morphology. In most cases, proliferating cells express both suppressor/cytolytic T-cell and natural killer (NK) cell surface markers, but other cell phenotypes may be observed. LGL-PD lymphocytes have been found to lack or show very low natural killer cell activity (NKa). The aim of the present paper is to investigate the underlying mechanisms responsible for impaired NKa in a homogeneous group of five selected LGL-PD patients with a CD3+, CD8+, CD57+ cell phenotype. RESULTS: In all patients, the expanded cell population expressed very low NKa against K562 cell targets, but this increased significantly with recombinant human interleukin-2 (rhIL-2) and phytohemagglutinin (PHA) activation. Recombinant human alpha-interferon (rhIFN-alpha) had no significant effect on NKa. Cells displayed normal tumor cell binding capacity but failed to release sufficient amounts of functionally active natural killer cytotoxic factor(s) (NKCFs) upon interaction with the NK-sensitive K562 cells targets. However, they did release soluble cytolytic molecules against K562 cells upon activation with PHA. CONCLUSIONS: Our findings provide evidence that the defective NKa in LGL-PD patients with the aforementioned phenotype is probably due, at least in part, to the inability of expanded lymphocytes to release NKCFs upon interaction with NK-sensitive cell targets. Since recognition of target cells by patient lymphocytes is not disturbed and the cells are capable of producing NKCFs upon activation with PHA, it is probable that the cause of this abnormality is located at the level of the activation signal provided by the stimulatory target cells. Studies in subcellular level are certainly needed for a more precise determination of the underlying defect.     

Fibroadenoma of the vulva. Report of a case

A case of fibroadenoma occurring in the vulva of a 24 year old woman is presented. This rare benign tumor appears as dermal or subcutaneous well circumscribed nodule. Histologically the fibroadenoma is characterized by epithelial and stromal proliferation. Two different concepts concerning histogenesis are cited; the authors believe that this tumor arises in ectopic mammary tissue.     

Studying electric field effects on embryonic myocytes

OBJECTIVE: Little attention has been paid to the occurrence of aortic regurgitation after complete repair in patients with pulmonary atresia and ventricular septal defect or tetralogy of Fallot. To highlight the development of aortic regurgitation or aortic root dilation severe enough to necessitate aortic valve replacement with or without aortic aneurysmorrhaphy or aortic root replacement, we retrospectively reviewed the records of patients who underwent aortic valve operation at our institution subsequent to repair of pulmonary atresia and ventricular septal defect or tetralogy of Fallot. METHODS: We searched the Mayo Clinic database for patients with pulmonary atresia and ventricular septal defect or tetralogy of Fallot who subsequently had aortic valve or aortic root operations. The degree of aortic regurgitation before operation was noted. Aortic sinus and root dimensions were measured. RESULTS: Sixteen patients underwent complete repair at a median age of 17 years, followed by an aortic operation a median of 13.5 years later. All 16 patients had dilated aortic sinuses at the time of the aortic valve operation. These 16 patients had aortic valve replacement: 11 with mechanical prostheses and 5 with bioprostheses. Five of the 16 also had reduction of aortic dilation by lateral aneurysmorrhaphy, and 1 had graft replacement of the ascending aorta. Five patients had associated conditions (evidence of valvular damage, recurrent ventricular septal defect, or history of endocarditis) discovered at the aortic valve operation that have been reported to be related to the development of aortic regurgitation. The remaining 11 patients had progressive aortic regurgitation despite complete, uncomplicated repair. CONCLUSIONS: Progressive aortic regurgitation and aortic root dilation can occur despite complete repair of pulmonary atresia and ventricular septal defect or tetralogy of Fallot.     

Relationship between soluble CD14, lipopolysaccharide binding protein, and the alveolar inflammatory response in patients with acute respiratory distress syndrome

The effects of bacterial endotoxin (lipopolysaccharide, LPS) are amplified by lipopolysaccharide binding protein (LBP) and CD14, resulting in cellular activation at very low concentrations of LPS. To investigate the importance of this pathway in acute lung injury, we measured LPS, LBP, and soluble CD14 (sCD14) in the bronchoalveolar lavage fluid (BAL) of 82 patients with acute respiratory distress syndrome (ARDS). LBP and sCD14 increased markedly in BAL of patients with ARDS. sCD14 and LBP each were strongly related to BAL total protein and polymorphonuclear neutrophil (PMN) concentration, whereas LPS concentration was not. Multivariate analyses showed sCD14 to be strongly related to BAL total protein, even after controlling for LPS and LBP concentrations. sCD14 was strongly and independently related to PMN concentration, after controlling for BAL LPS, LBP, and interleukin-8 (IL-8). The BAL LPS concentration was not strongly related to either BAL total protein or BAL PMN. The BAL sCD14 and LBP values were similar in all subgroups of patients with ARDS, and were not related to survival. The serum LBP and sCD14 were elevated in ARDS, but were not related to BAL total protein, LBP, sCD14, PMN, or clinical outcome. Thus, LBP and sCD14 reach high concentrations in the lungs of patients with ARDS, and BAL sCD14 is strongly related to two major indices of lung inflammation: total protein and PMN concentration. CD14-dependent mechanisms may contribute to lung inflammation in ARDS.     

Ofloxacin-induced seizure

OBJECTIVE: To describe a possible case of ofloxacin-induced generalized tonic-clonic seizure. Although the etiology is unknown, ofloxacin most likely precipitated this patient's seizure threshold because of sepsis or secondary to drug accumulation due to the patient's compromised renal function. CASE SUMMARY: A 69-year-old white woman with non-small-cell lung cancer and a history of central nervous system metastatic disease treated with radiation therapy presented to the emergency department with symptoms of urosepsis. Because of multiple drug allergies she was started on ofloxacin (hospital formulary quinolone). After 4 days of therapy she developed a generalized tonic-clonic seizure. A computed tomography scan of the head with and without contrast was negative. The ofloxacin was discontinued and aztreonam therapy was started. Phenytoin therapy was instituted and, despite serum concentrations below the conventional therapeutic range, there was no recurrence of seizure. Subsequent discontinuation of phenytoin did not result in a seizure for this patient. DISCUSSION: Seizures induced by the fluoroquinolones are uncommon. The histopathologic features of this phenomenon are currently unknown. In this patient, imaging studies were negative for structural defects, ruling out metastasis as the cause of the seizure. Therefore, an investigation of drug-related causes ensued. The most likely offending agent was ofloxacin. Ofloxacin has been reported in the literature as a cause of seizures in patients with compromised renal function. CONCLUSIONS: This case and other reports indicate that fluoroquinolones, including ofloxacin, may contribute to seizure development in patients with or without a history of epilepsy. Fluoroquinolone therapy should be used with caution in patients with risk factors for the development of drug-induced seizures.     

DdlN from vancomycin-producing Amycolatopsis orientalis C329.2 is a VanA homologue with D-alanyl-D-lactate ligase activity

Vancomycin-resistant enterococci acquire high-level resistance to glycopeptide antibiotics through the synthesis of peptidoglycan terminating in D-alanyl-D-lactate. A key enzyme in this process is a D-alanyl-D-alanine ligase homologue, VanA or VanB, which preferentially catalyzes the synthesis of the depsipeptide D-alanyl-D-lactate. We report the overexpression, purification, and enzymatic characterization of DdlN, a VanA and VanB homologue encoded by a gene of the vancomycin-producing organism Amycolatopsis orientalis C329.2. Evaluation of kinetic parameters for the synthesis of peptides and depsipeptides revealed a close relationship between VanA and DdlN in that depsipeptide formation was kinetically preferred at physiologic pH; however, the DdlN enzyme demonstrated a narrower substrate specificity and commensurately increased affinity for D-lactate in the C-terminal position over VanA. The results of these functional experiments also reinforce the results of previous studies that demonstrated that glycopeptide resistance enzymes from glycopeptide-producing bacteria are potential sources of resistance enzymes in clinically relevant bacteria.