Scanning electron microscopy comparing exclamation mark hairs in alopecia areata with normal hair fibres, mechanically broken by traction

A scanning electron microscope was used to compare the distal ends of exclamation mark hairs from alopecia areata patients with the fracture surface of normal hair fibres, mechanically broken by traction. The exclamation mark hairs shows minimal damage to the cuticular cell pattern of the hair shaft. Where the cuticle was absent, cortex and medulla showed low-density features fanning out into a fringe-like structure at the distal ends. The fracture surfaces of normal hair fibres, mechanically broken by traction showed a markedly abnormal cuticular scale pattern, whereas the features of cortical and medullary tissue were normal. These morphological differences between the fracture surface of exclamation mark hairs and normal hair fibres, mechanically broken by traction, may enhance our understanding of the pathogenesis of alopecia areata.     

Actin polymerization and its relationship to locomotion and chemokinetic response in maturing human promyelocytic leukemia cells

We studied actin polymerization in the HL-60 human promyelocytic leukemia cell line during induced myeloid maturation and its relationship to the rate of locomotion (ROL). The percent G-actin (of total actin) was measured by DNAase I inhibition, F-actin was determined by fluorescence-activated cell sorter (FACS) analysis of nitrobenzoxadiazol (NBD)-phallacidin-stained cells, and ROL was measured by computer-assisted analysis of the tracks of individual cells. Uninduced HL-60 cells moved slowly (2.3 +/- 1.0 microns/min) and showed no change in ROL or in the state of actin polymerization when stimulated by formyl-methionyl-leucyl-phenylalanine (fMLP). Nonstimulated cells induced to differentiate with dimethylformamide had no change in the degree of actin polymerization but exhibited a mean (m) ROL similar to normal human polymorphonuclear leukocytes (PMN) (8.6 +/- 1.4 micron/min [HL-60 cells] v 7.8 +/- 1.8 microns/min [PMN]. When induced HL-60 cells were stimulated with fMLP, actin polymerization occurred. The F-actin content increased, as determined by FACS analysis of NBD-phallacidin-stained cells, and the percentage of G-actin decreased, as determined by a 24.5% decrease in DNAase I inhibitory activity. However, induced HL-60 cells stimulated with fMLP did not increase their mROL. These studies show that, unlike normal human PMN, chemotactic peptides can cause an intracellular biochemical change that is not associated with a chemokinetic response in induced HL-60 cells. The HL-60 cell line may be a useful model to study the development of chemotactic peptide-mediated actin polymerization during myeloid cell maturation.     

Renal Effects of Acute Exposure to Toluene

ABSTRACT. Urinary excretion rates of β₂-microglobulin and albumin were measured in 43 male printing trade workers and 43 age-matched male controls before and during exposure to toluene, 382 mg/m³, for 6¹/₂ hours in a climate chamber. There were no significant changes in renal excretion rates of albumin and β₂-microglobulin during toluene exposure indicating that no causal relationship exists between moderate exposure to organic solvents and renal injury.     

刺激剂类药物及代谢物的分离鉴定

报道了41种刺激剂的气相色谱和质谱数据以及人尿中原药和它们的游离型和结合型代谢物的分离和鉴定方法。用分辨率高的毛细管气相色谱分离,以灵敏度高专属性好的氮磷检测器检测志愿者24 h尿样中游离型母体药及代谢物。选择部分时间收集尿样进行直接气质联用分析以及采用三氟醋酰化、三甲基硅烷化和两者并用的衍生化方法鉴定母体药及游离型代谢物。尿样酸水解后,再进行以上选择性衍生化,可测定它们的结合型代谢物。     

Normal and abnormal temporomandibular joint: MR imaging with surface coil

The normal temporomandibular joint (TMJ) was evaluated using magnetic resonance (MR) imaging with a surface coil in five subjects and compared with the abnormal joint in 37 patients (aged 14-59 years; total joints studied, 76). Multisection 3-mm-thick sagittal, coronal, and axial images were obtained with a 1.5-T MR system and 6.5-cm-diameter surface coil using both partial saturation and spin-echo sequences (TR = 1,000 msec, TE = 20 or 25 msec). A comparison with arthrography (n = 13 joints), computed tomography (CT) (n = 11), and surgical (n = 5) findings demonstrated that MR imaging with a surface coil provided an accurate depiction of both normal and abnormal TMJs. MR provided information about meniscal position, morphology, and histology that was not available with either arthrography or CT alone. The imaging potential of MR and its noninvasive characteristics warrant priority for further examination of MR as a useful modality in the diagnosis of TMJ pain and dysfunction.     

Murine eosinophils labeled with indium-111 oxine: localization to delayed hypersensitivity reactions against a schistosomal antigen and to lymphokine in vivo

We have evaluated a method for quantitation of eosinophil migration to stimuli in vivo. Upon transfusion into normal syngeneic mice, 111In- labeled eosinophils had an intravascular half-life of 9.5 hr and distributed predominantly into spleen, bone marrow, and liver. In either Schistosoma mansoni-infected mice or recipients of lymphoid cells from infected mice, intradermal (ear pinna) injection of the schistosomal egg antigenic preparation (SEA) elicited time-dependent accumulation of 111In-labeled eosinophils detectable by either gamma scintillation counting of tissue samples or by nuclear medicine external imaging. Intradermal administration of a lymphokine fraction (containing eosinophil stimulation promoter activity) similarly caused accumulation of 111In-labeled eosinophils. Both reactions depended on the concentration of stimulus (SEA or lymphokine). 111In-labeled neutrophils or macrophages or 125I-albumin did not preferentially accumulate at the reactions examined to the extent found with 111In- labeled eosinophils, indicating that localization of label depends on an active process and is due to eosinophils rather than a contaminating cell type. The method was used to estimate how long eosinotactic lymphokine remained at dermal sites: 60% of initial activity was present 12 hr after injection. The model is discussed with regard to the role of lymphokines in hypersensitivity reactions with eosinophil involvement, such as the granulomatous response to S. mansoni eggs.     

A chromosome with five gamma-globin genes

Globin gene mapping of DNA from a Black newborn resulted in the detection of a chromosome with five gamma-globin genes. Based on results from digests with enzymes EcoRI and PstI, we concluded that the three genes between the 5'G gamma and 3'A gamma genes are G gamma genes with a possible 5' segment derived from A gamma. The high G gamma level in the fetal hemoglobin (Hb F) of the baby is consistent with this view. Family relationships were such that speculation as to the mechanism causing this quintuplication of the gamma-globin genes was not possible.     

HLA and duodenal ulcer in The Netherlands

Eighty-one Dutch patients with a duodenal ulcer (DU) were tested with respect to 24 HLA antigens. There was no significant difference in the distribution of HLA antigens between the DU patients and the controls. However, none of the 22 patients younger than thirty years at the onset of symptoms had HLA-Bw35, whereas among the 59 patients aged between thirty and eighty at the onset of symptoms, twelve had this antigen.     

Acetylcholine release in myasthenia gravis: Regulation at single end-plate level

In myasthenia gravis, loss of acetylcholine receptors at motor end-plates is induced by antireceptor autoantibodies. At end-plates in rats in which myasthenia gravis–like symptoms are induced by chronic treatment with α-bungarotoxin, acetylcholine release is increased. Within muscles from such rats there is a strong correlation between the increase of acetylcholine release at an end-plate and the loss of postsynaptic acetylcholine receptors, caused by the toxin. The question is whether upregulation of acetylcholine release is a clinically relevant compensatory mechanism in myasthenia gravis or only a feature of the animal model using α-bungarotoxin. We investigated electrophysiologically the in vitro acetylcholine release at end-plates of muscles from patients with myasthenia gravis and rats with experimental autoimmune myasthenia gravis where acetylcholine receptor reduction is caused by autoantibody attack. In both human and rat autoimmune myasthenic muscle, the mean quantal content was considerably increased compared with control levels. At each individual myasthenic end-plate, the increase in quantal content appeared to be correlated with the reduction of the amplitude of the miniature end-plate potential. This finding suggests the existence of an important compensatory mechanism in myasthenia gravis, in which retrograde acting factors (i.e., from muscle fiber to nerve terminal) upregulate acetylcholine release.