九寨沟景区急诊病例疾病谱调查

目的探讨九寨沟景区急诊患者疾病谱流行病学特点,提高九寨沟景区急诊患者的诊治水平。方法对2013年1~12月四川省九寨沟县人民医院14 196例急诊病例资料进行回顾性分析。结果院前急诊病种排序在前4位的是呼吸系统疾病、高原反应、损伤、心脑血管疾病,呼吸系统疾病患病比例最高,达60.44%;呼吸系统疾病、高原反应、损伤发生率女性高于男性,心脑血管疾病发生率男性明显高于女性;高原反应、损伤、心脑血管疾病以60岁以上人群为主。结论在类似九寨沟这种高寒景区,老年旅游者需要特别重视对呼吸系统疾病、高原反应、损伤、心脑血管疾病的预防。     

The effects of tumor-promoting phorbol esters on human granulopoiesis in vitro

In order to determine whether the tumor-promoting phorbol esters are capable of inducing normal human committed granulocytic-monocytic progenitor cells (CFUc) to proliferate and differentiate in the absence of granulocyte-monocyte colony-stimulating activity (CSA), we studied the effects of these compounds on human granulopoiesis in vitro. We found that when light-density human marrow cells or peripheral blood leukocytes were depleted of adherent cells and then incubated in semisolid tissue culture medium under conditions optimal for CFUc growth, phorbol myristate acetate (PMA) and its congeners produced no measurable stimulatory effect on the proliferation of CFUc in the absence of added CSA. Likewise, when light-density marrow cells that had not been depleted of adherent cells were plated in the cultures, no stimulation of CFUc colony growth resulted from the addition of PMA. However, when light-density peripheral blood leukocytes were used as a target source of CFUc without first subjecting them to adherence separation, enhanced proliferation and differentiation of CFUc were noted in cultures that contained PMA. To investigate the possibility that CSA production by monocytes in these cultures in response to activation by PMA might account for the enhanced colony formation that we observed, we incubated isolated peripheral blood monocytes in short- term liquid suspension cultures and found that in the presence of PMA, large quantities of CSA were secreted into the surrounding medium. Finally, we noted that when marrow cell suspensions were suboptimally stimulated by low concentrations of CSA added to the cultures, the effects of PMA on CFUc proliferation were unpredictable, enhancing colony formation in some cases and inhibiting it in others. Our data indicate that although the tumor-promoting phorbol esters do not appear capable of directly stimulating the proliferation or differentiation of human CFUc in the absence of CSA, they may do so indirectly by causing auxiliary cells such as monocytes to secrete CSA.     

Tumor necrosis factor-alpha and FMLP receptors are functionally linked during FMLP-stimulated activation of adherent human neutrophils

Human peripheral blood neutrophils (PMN) plated onto fibrinogen and activated with FMLP release H2O2 and lactoferrin, a specific granule component, with parallel kinetics. Although tumor necrosis factor-alpha (TNF alpha) only primes PMN in suspension, it is a potent agonist of adherent PMN. Activation of adherent PMN by FMLP (10(-7) mol/L) stimulated detectable release of TNF alpha within 45 minutes of stimulation, with maximal release (45.5 pg/10(6) cells) detected by 90 minutes. TNF alpha release paralleled the release of both lactoferrin and H2O2. To determine if TNF alpha plays a role in H2O2 and lactoferrin release, we investigated the effect of anti-TNF alpha antibodies on FMLP-stimulated activation of adherent PMN. A neutralizing rabbit anti-TNF alpha antibody inhibited both H2O2 and lactoferrin release stimulated by FMLP, whereas rabbit lgG, anti-HLA- A,B,C, anti-CD 14, and anti-interleukin-8 antibodies were without effect. The simultaneous addition of TNF alpha (1,000 U/mL) with anti- TNF alpha antibody reversed the inhibition seen with anti-TNF alpha alone. Furthermore, treatment of PMN with either actinomycin D or cylcoheximide resulted in partial (33%) inhibition of H2O2 and lactoferrin release, suggesting that protein synthesis is required for FMLP-mediated activation of adherent PMN. The addition of TNF alpha to either cycloheximide or of actinomycin D-treated PMN overcame the inhibition, indicating that the effect was specific for TNF alpha. The addition of antibodies against either the 55-or 75-kD TNF alpha receptors (referred to as p55 and p75, respectively) resulted in partial (32%) inhibition of FMLP-mediated activation of H2O2 and lactoferrin release, whereas a combination of both antibodies reduced their release to control levels. These data indicate that both p55 and p75 are involved in FMLP activation of adherent PMN. Taken together, these findings indicate that the production of TNF alpha and ligation of TNF alpha receptors are central to FMLP activation of PMN adherent to fibrinogen.     

改良皮内注射法在新生儿卡介苗接种中的应用

目的探讨改良皮内注射法提高新生儿卡介苗接种成功率的效果。方法将136例符合接种条件的新生儿随机分成2组，实验组66例采用改良皮内注射手法接种卡介苗，对照组70例采用常规皮内注射法接种卡介苗，比较2组的接种效果。结果实验组接种一次成功率，新生儿卡介苗接种后12周卡痕率、结核菌素纯蛋白衍化物（PPD）试验阳性率，均高于对照组，2组比较差异有统计学意义，P〈0．01。结论改良皮内注射法应用于新生儿卡介苗接种，具有不漏液，皮丘大小符合接种要求，接种成功率高的优点。     

Plasma Levels of Natriuretic Peptides During Ventricular Pacing in Patients with a Dual Chamber Pacemaker

The mechanism(s) responsible for the release of brain natriuretic peptide (BNP), a cardiac hormone of ventricular origin, are still not completely understood. We measured plasma atrial natriuretic peptide (ANP) and BNP in 15 subjects (10 men, mean age 67 ± 3 years) with a dual chamber pacemaker and unimpaired heart function during ventricular pacing, which is known to induce an increase in atrial pressure and plasma ANP concentration. Under ECC monitoring, all subjects received sequential atrioventricular pacing for 30 minutes and ventricular pacing for 30 minutes, at the same rate of 80 beats/min. Arterial pressure and plasma BNP and ANP levels were measured every 10 minutes throughout the study. Ventricular pacing led to atrioventricular dissociation in eight subjects and to retrograde ventriculo-atrial conduction in seven. Arterial pressure remained unchanged in all subjects. In the group with atrioventricular dissociation, plasma ANP increased from 10.14 ± 0.58 to 16.72 ± 0.92 fmol/mL at the 60th minute (P < 0.0001), whereas plasma BNP did not change at all (fiom 1.26 ± 0.07 to 1.16 ± 0.09 fmol/mL). In the group with retrograde conduction, plasma ANP concentration doubled (fiom 10.95 ± 1.66 to 21.40 ± 1.51 fmol/mL, P < 0.0001), BNP increased 1.5-fold (from 1.16 ± 0.06 to 1.64 ± 0.14 fmol/mL, P < 0.001), and the ANP: BNP ratio augmented fiom 10:1 to 13.4:1. These results indicate that the release of ANP and BNP is regulated by different mechanisms, supporting the view that there is a dual natriuretic peptide system, comprising ANP fiom the atria and BNP fiom the ventricles.     

Lack of effect on platelet increments of granulocyte-macrophage-colony- stimulating factor following autologous bone marrow transplantation for malignant lymphoma

BACKGROUND: Recombinant growth factors are used increasingly often to stimulate bone marrow recovery after intensive chemotherapy and bone marrow transplantation. Their effects on the requirements for and responsiveness to coincident therapies, including transfusion, should be defined. STUDY DESIGN AND METHODS: To determine whether treatment with recombinant granulocyte-macrophage-colony-stimulating factor (GM- CSF) affects platelet transfusion responsiveness, the clinical and blood bank records were examined for 16 adult patients (8 controls, 8 receiving GM-CSF) participating in a double-blind study of GM-CSF administration (250 micrograms/m2 × 21 days) following autologous bone marrow transplantation for lymphoma. For each platelet transfusion, a corrected count increment was calculated, and note was made of the presence or absence of selected additional factors thought to decrease platelet responsiveness: fever, amphotericin treatment, HLA antibodies, platelet ABO incompatibility, and febrile transfusion reactions. RESULTS: The total number of platelet transfusions (GM-CSF patients, 145; controls, 145) and the mean number of transfusions per patient (GM- CSF, 18.3; controls, 18.0) were comparable in the two groups. GM-CSF patients received significantly more platelets that were ABO incompatible, that were given during a febrile period, or that were given while the patient was on amphotericin. Nevertheless, the corrected count increments in patients who received GM-CSF were at least as good as those in controls: for GM-CSF patients: mean was 8,574 +/− 5,868, median was 7,818, 49 percent were < 7,500 and 66 percent were < 10,000; for controls; mean was 7,618 +/− 7,536, median was 6,100, 59 percent were < 7,500, and 73 percent were < 10,000. CONCLUSION: In this group of patients, GM-CSF did not adversely affect the required number of, increments to, or incidence of refractoriness to platelet transfusions.     

T lymphocytes in skin lesions of psoriasis and mycosis fungoides express B7-1: a ligand for CD28

The activation of T cells requires two distinct signals. One signal involves interaction of the antigen-specific T-cell receptor with major histocompatibility complex molecules plus antigenic peptide; a second signal, which is antigen nonspecific, is the interaction of CD28 with its natural ligands B7-1 and B7-2/B70. CD28 is expressed on 80% of T cells, is upregulated after activation, and binds to B7 gene-family members, found on antigen-presenting cells. Because of our interest in the immunologic basis of benign and malignant T-cell-mediated disorders of the skin, we investigated the cellular distribution of CD28 and B7 family members in lesions of psoriasis and mycosis fungoides. By immunostaining cryostat sections of skin, CD28 was found to be expressed on virtually all lymphocytes in the epidermis and dermis of both skin diseases. Surprisingly, B7-1 was also found to be expressed on virtually all lymphocytes in the epidermis and dermis of both skin diseases. B7-1 expression was confirmed on CD3+ T lymphocytes using flow cytometry of single cell suspensions of fresh, unfixed psoriatic lesional tissue. To exclude the possibility that this result was caused by a second reagent contaminating the monoclonal antibody (MoAb) preparation, two different lots were used, and the MoAb was absorbed onto Chinese hamster ovary (CHO) transfectants expressing B7-1, or vector-only transfected CHO cells. These procedures confirmed that a B7- 1-like epitope was being recognized on psoriatic lesional T cells. In contrast to B7-1 expression on lymphocytes, B7-3, as defined by anti-BB- 1 MoAb reactivity, was found primarily on epidermal keratinocytes in both skin diseases and was not found on T cells. These results indicate that within two common skin disorders, lesional T cells accumulate in the dermis and epidermis, which express B7-1. Such expression may permit self-costimulation involving the CD28-mediated activation pathway, and thereby contribute to the ongoing T-cell proliferation present in these chronic, benign, and malignant skin diseases.     

CD34+ endothelial cell lines derived from murine yolk sac induce the proliferation and differentiation of yolk sac CD34+ hematopoietic progenitors

Embryonic hematopoiesis is initiated in part in the blood islands of the yolk sac. Previous confocal microscopic analysis has shown that the CD34 antigen, a mucin-like cell surface glycoprotein that is expressed by hematopoietic progenitors and all endothelial cells of the adult and embryo, is also found on a subset of luminal hematopoietic-like cells in the yolk sac blood islands as well as on the vascular endothelium lining these early hematopoietic locations. We show here that, as in all other hematopoietic sites thus far examined, immunoaffinity- purified CD34+ nonadherent cells from murine yolk sacs contain the vast majority of erythroid and myeloid progenitor cell colony forming activity. To examine the developmental interactions between these CD34+ hematopoietic progenitor cells of the yolk sac and the CD34+ yolk sac endothelium, we have immunaffinity-purified adherent endothelial cells from day 10.5 yolk sacs using CD34 antiserum and produced cell lines by transformation with a retrovirus expressing the polyoma middle T antigen. Analysis of these cell lines for CD34, von Willebrand's factor, FLK 1 and FLT 1 expression, and capillary growth in Matrigel indicates that they appear to be endothelial cells, consistent with their original phenotype in vivo. Coculture of yolk sac CD34+ hematopoietic cells on these endothelial cell lines results in up to a 60-fold increase in total hematopoietic cell number after approximately 8 days. Analysis of these expanded hematopoietic cells showed that the majority were of the monocyte/macrophage lineage. In addition, examination of the cultures showed the rapid formation of numerous cobblestone areas, a previously described morphologic entity thought to be representative of early pluripotential stem cells. Scrutiny of the ability of these endothelial cell lines to expand committed progenitor cells showed up to a sixfold increase in erythroid and myeloid colony- forming cells after 3 to 6 days in culture, consistent with the notion that these embryonic endothelial cells mediate the expansion of these precursor cells. Polymerase chain reaction analyses showed that most of the cell lines produce FLK-2/FLT-3 ligand, stem cell factor, macrophage colony-stimulating factor, leukemia-inhibitory factor, and interleukin- 6 (IL-6), whereas there is a generally low or not measurable production of granulocyte colony-stimulating factor, granulocyte-macrophage colony- stimulating factor, IL-1, IL-3, transforming growth factor beta-1, erythropoietin, or thrombopoietin. The output of mature hematopoietic cells from these cocultures can be modified to include an erythroid population by the addition of exogenous erythropoietin. These data suggest that endothelial cell lines derived form the yolk sac provide an appropriate hematopoietic environment for the expansion and differentiation of yolk sac progenitor cells into at least the myeloid and erythroid lineages.