乐胃煎逆转胃癌前病变AgNOR及细胞图像分析

目的研究乐胃煎逆转胃癌前病变不完全结肠型肠化和／或中度异型增生的疗效．方法胃镜病理证实为不完全结肠型肠化和／或中度异型增生４６例．治疗组３０例用乐胃煎，对照组１６例用德诺（Ｄｅ＿Ｎｏｌ）．治疗前后胃镜活检胃窦固定部位粘膜标本作ＡｇＮＯＲ染色及细胞图像分析．结果乐胃煎对不完全结肠型肠化及中度异型增生总有效率均高于Ｄｅ＿Ｎｏｌ，分别为７２％比２５％（Ｐ＜００５）和８９５％比４４４％（Ｐ＜００５）．乐胃煎治疗前后，ＡｇＮＯＲ计数分别为７３０±１１６和４８１±１５０（Ｐ＜００１），Ｄｅ＿Ｎｏｌ组为７７３±０９２和７０５±１０２（Ｐ＜００１）．两组治疗前后ＡｇＮＯＲ计数差值均数相比，统计学上也有显著性差异，分别为２５２±１５４和０６９±０４８（Ｐ＜００１）．乐胃煎组中２０例作细胞图像分析，治疗后各参数（长轴、短轴、核浆比、结构异型指数等）均有不同程度的降低，有显著性差异．结论乐胃煎确有较好地逆转胃癌前病变的功效．     

Hematologic and immunomodulatory effects of an interleukin-1 receptor antagonist coinfusion during low-dose endotoxemia in healthy humans

Endotoxin is a component of gram-negative bacteria that causes hematologic and immunologic changes through its induction of cytokines. Interleukin-1 receptor antagonist (IL-1Ra) is a naturally occurring inhibitor of IL-1 that competes with IL-1 for occupancy of cell-surface receptors but possesses no agonist activity. We investigated the ability of human recombinant IL-1Ra to block the effects of low-dose endotoxin. Fourteen healthy male volunteers between 18 and 30 years old were injected intravenously with 3 ng/kg Escherichia coli endotoxin. Concurrent with the injections, nine volunteers received a 3-hour continuous intravenous infusion of IL-1Ra. The other five subjects were given a 3-hour infusion of saline. Volunteers injected with endotoxin experienced a threefold increase in circulating neutrophils over baseline. This neutrophilia was significantly reduced by 48% in subjects administered endotoxin plus IL-1Ra (P = .0253). Ex vivo mitogen-induced peripheral blood mononuclear cell proliferation decreased by greater than 60% at 3 and 6 hours after endotoxin injection (P = .0053). This endotoxin-induced reduction in mitogen response was reversed in subjects coinjected with IL-1Ra (P = .0253). Endotoxin-induced symptoms, fever, and tachycardia were unaffected by IL-1Ra. IL-1 appears to be an important mediator in endotoxemia because some of its hematologic and immunomodulatory effects can be blocked by IL-1Ra.     

The 14q+ chromosome in pre-B-ALL

A child who had acute lymphoblastic leukemia (ALL) associated with an 8;14 chromosome translocation and with a pre-B phenotype is described. The leukemic cells were determined to be pre-B-cells on the basis of intracytoplasmic mu-chain immunoglobulin (cIgM+) and the common-ALL antigen, lack of receptors for sheep erythrocytes, and lack of surface immunoglobulin. The 8;14 translocation is frequently found in patients with Burkitt's lymphoma and in most patients with B-cell ALL and is known to carry a poor prognosis. Thus far, no karyotypes have been reported for patients with pre-B-ALL. The present case indicates that a 14q+ chromosome may provide a proliferative advantage not only to cells with a B-cell phenotype, but also to pre-B-cells. The short survival of our patient also suggests that the 14q+ abnormality and the pre-B phenotype may signal a poor prognosis.     

Acute injury of the ligaments of the knee: magnetic resonance evaluation

Eleven acutely injured knees and 13 normal knees were examined by magnetic resonance imaging (MRI) to assess the value of this modality in detecting acute ligamentous injury of the knee. The presence of torn ligaments in the injured knees was determined by arthroscopy and/or arthrotomy in ten cases and clinical follow-up in one case. The anterior and posterior cruciate ligaments (ACL and PCL) were demonstrated by sagittal spin echo (SE) images through the intercondylar notch (TE = 30 ms; TR = 2,000 ms). The tibial and fibular collateral ligaments (TCL and FCL) were evaluated on coronal SE images (TE = 30 ms, TR = 200 or 530 ms; TE = 120 ms, TR = 2,000 or 2,120 ms). The ACL and PCL were considered torn on MR if they appeared disrupted or were not seen in their normal anatomical positions. The collateral ligaments were considered torn if abnormal high-intensity signal was noted in adjacent soft tissues on TE = 120 ms images or if disruption of a ligament was apparent. Eleven of 15 torn ligaments and 80 of 81 normal ligaments were correctly identified by these criteria. It is concluded that MR imaging may be useful in detecting acute injury of ligaments of the knee.     

Impaired inhibitory G-protein function contributes to increased calcium currents in rats with diabetic neuropathy

There is a growing body of evidence that sensory neuropathy in diabetes is associated with abnormal calcium signaling in dorsal root ganglion (DRG) neurons. Enhanced influx of calcium via multiple high‐threshold calcium currents is present in sensory neurons of several models of diabetes mellitus, including the spontaneously diabetic BioBred/Worchester (BB/W) rat and the chemical streptozotocin (STZ)‐induced rat. We believe that abnormal calcium signaling in diabetes has pathologic significance as elevation of calcium influx and cytosolic calcium release has been implicated in other neurodegenerative conditions characterized by neuronal dysfunction and death. Using electrophysiologic and pharmacologic techniques, the present study provides evidence that significant impairment of G‐protein‐coupled modulation of calcium channel function may underlie the enhanced calcium entry in diabetes. N‐ and P‐type voltage‐activated, high‐threshold calcium channels in DRGs are coupled to mu opiate receptors via inhibitory G(o)‐type G proteins. The responsiveness of this receptor coupled model was tested in dorsal root ganglion (DRG) neurons from spontaneously‐diabetic BB/W rats, and streptozotocin‐induced (STZ) diabetic rats. Intracellular dialysis with GTPgammaS decreased calcium current amplitude in diabetic BB/W DRG neurons compared with those of age‐matched, nondiabetic controls, suggesting that inhibitory G‐protein activity was diminished in diabetes, resulting in larger calcium currents. Facilitation of calcium current density (I(DCa)) by large‐amplitude depolarizing prepulses (proposed to transiently inactivate G proteins), was significantly less effective in neurons from BB/W and STZ‐induced diabetic DRGs. Facilitation was enhanced by intracellular dialysis with GTPgammaS, decreased by pertussis toxin, and abolished by GDPbetaS within 5 min. Direct measurement of GTPase activity using opiate‐mediated GTPgamma[(35)S] binding, confirmed that G‐protein activity was significantly diminished in STZ‐induced diabetic neurons compared with age‐matched nondiabetic controls. Diabetes did not alter the level of expression of mu opiate receptors and G‐protein alpha subunits. These studies indicate that impaired regulation of calcium channels by G proteins is an important mechanism contributing to enhanced calcium influx in diabetes.