Peripheral blood responses in elderly patients with some prevalent diseases

The aim of the research was to study blood responses to inflammatory processes in patients of different ages. The subjects of the study were 31 healthy persons and 198 patients, 116 of whom had pneumonia and 82 had chronic pyelonephritis. The patients were divided into three age groups: 16 to 39 years, 40 to 59 years, and older than 60 years. The following parameters were calculated on the basis of peripheral blood leukocyte composition and ESR: leukocyte intoxication index (LII), lymphocyte index (LymI), leukocyte shift index (LSI), leukocyte index (LI), leukocyte to ESR ratio index (LESRRI), lymphocyte-granulocyte index (LGI), total index (TI), neutrophile to lymphocyte ratio index (NLymRI), neutrophile to monocyte ratio index (NMRI), and lymphocyte to monocyte ratio index (LMRI). The majority of the indexes (LII, LymI, LSI, LI, LESRRI, LGI, and LMRI) in acute inflammation processes and some of them (LESRRI, NLymRI, and LMRI) in chronic inflammation altered significantly in all the age groups, which demonstrated that compensatory and adaptive mechanisms remained preserved in the elderly. The were age-dependent differences in blood responses to inflammation: LymI, LI, and LGI were significantly lower in the elderly with chronic pyelonephritis, whereas in Groups 1 and 2 there were no changes; NMRI was decreased in Groups 1 and 2 in chronic pyelonephritis and did not differ from the elderly controls. In acute inflammation, there were no significant differences from the controls in NlymRI in Group 3, while this parameter in Groups 1 and 2 differ from that in the controls. Thus, hematological indices make it possible to assess the work of effectory mechanisms of the immune system, the degree of their compensation in patients belonging to different age groups.     

Microtiter plate assay for phagocyte-derived taurine-chloramines.

Despite their potential importance, the role of phagocyte-derived chloramines ("long-lived oxidants") has not yet been investigated in inflammatory or infectious diseases. We have developed a sensitive spectrophotometric microtiter plate assay for chloramines based on their capacity to oxidize potassium iodide (KI). Consistent levels of endogenous chloramines were detected in normal human polymorphonuclear neutrophil (PMN) supernatants after stimulation by phorbol myristate acetate (PMA) or opsonized zymosan. Exogenous taurine strongly enhanced chloramine secretion and was used to quantify the chlorinating potential of PMN. Taurine-chloramines were also detectable in monocyte supernatants, although in smaller amounts. The specificity of the KI assay was assessed both in terms of effect of compounds inhibiting (KBr) or interacting with (sodium azide and catalase) chloramine formation and by showing that PMN from patients with chronic granulomatous disease, due to a hereditary lack of oxidative response capacity, were unable to produce chloramines. Taurine-chloramine levels secreted by PMA (but not zymosan)-stimulated PMN were closely related to the cellular luminol-amplified chemiluminescence (CL) responses although the CL assay failed to detect chloramines in PMN supernatants. We consider that this KI assay should be of use in studying the role of long-lived phagocyte-derived oxidants in clinical medicine.     

Increased chemiluminescence of polymorphonuclear leucocytes from patients with progressive systemic sclerosis

Chemiluminescence (CL) of whole blood and isolated polymorphonuclear leucocytes (PMN) from patients with systemic sclerosis (SS) and from age and sex matched controls was measured. CL was induced by the addition of particles (zymosan, latex beads), or phorbol myristate acetate (PMA) or chemotactic peptide (FMLP). Whole blood CL (induced by PMA, zymosan or latex particles) was significantly greater in SS patients than in normal controls. Isolated PMN CL (induced by PMA, FMLP or latex particles) was also significantly greater in the SS patients compared with controls. Increased CL or PMN from patients with SS was mainly observed when luminol was used as amplifier (which detects hydrogen peroxide formation). In most cases, lucigenin-amplified CL of PMN from patients with SS (which detects the primary superoxide anion radical formation) did not differ from the controls. Sera from patients with SS significantly increased both spontaneous and induced CL of normal PMN. Enhanced excitability of PMN to phagocytosis-related stimuli may provide a mechanism for the (leucocyte-mediated) endothelial injury in SS.     

Coronary heart disease in the elderly

In 1984, 435,759 deaths were attributed to CHD among persons greater than or equal to 65 years of age. CHD was the leading cause of death in this group. Death rates rose steeply with age among the elderly. Men had higher death rates than women, but the male-to-female ratio declined with increasing age. Considerable geographic variation in CHD mortality in the elderly was noted. Since 1968, CHD death rates have declined in persons greater than or equal to 65 years of age in each age, sex, and race group. However, prevalence of self-reported CHD in the elderly population has increased. Prevalence rates increased with age except for a slight decrease above age 75 in men. In 1985, 436,000 persons aged greater than or equal to 65 years were discharged with a principal diagnosis of acute MI. The hospital case fatality rate was 21.8%. Since 1970, hospitalization rates for acute MI have generally increased, while hospital fatality rates have decreased for persons greater than or equal to 65 years of age. Since 1979, utilization of coronary artery bypass surgery and coronary arteriography have dramatically increased among the elderly. In 1980 and 1981, elderly persons made six million visits to physicians' offices for chronic CHD. CHD contributed importantly to the 1980 expenditures of 3.3 billion dollars in men and 4.8 billion dollars in women greater than or equal to 65 years of age for heart disease care. Although mortality rates from CHD in the elderly have decreased since 1968, increasing hospitalization rates and utilization of other health care services emphasize the need for more vigorous efforts at prevention.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impairment of polymorphonuclear leukocyte function and metabolic control of diabetes.

OBJECTIVE--In this study, ingestion of Staphylococcus aureus and "bacteria killing" (BK) were measured to evaluate polymorphonuclear leukocyte (PMN) phagocytic functions and chemiluminescence response (CL) to phorbol-myristic acetate (PMA) as respiratory burst activity with regard to metabolic control parameters in diabetic patients. RESEARCH DESIGN AND METHODS--PMN phagocytic functions were assessed in 40 diabetic patients, all receiving insulin and in poor metabolic control, with 3H-thymidine-labeled Staphylococcus aureus in a modified radiometric assay. Bacteria killing was determined by pure-plate counting of surviving bacteria (colony-forming units [cfu]) and luminol-enhanced CL in response to PMA as a measure of respiratory burst. PMN function data were correlated to HbA1 as parameter of recent metabolic control. RESULTS--PMN of diabetic patients showed a significant reduction in Staphylococcus aureus (50.7 +/- 4.1%) and BK (29.4 +/- 4.2%) compared with healthy nondiabetic control subjects (76.6 +/- 4.6% and 16.3 +/- 3.1%, respectively, P less than 0.001), and PMN CL response was markedly reduced in diabetic patients also. Linear regression analysis showed a highly significant negative correlation of HbA1 versus Staphylococcus aureus (r = -0.67, P = 0.001) and a positive correlation for BK (r = 0.73, P less than 0.001). This was also true for CL, although this did not reach statistical significance (P = 0.06). CONCLUSIONS--The data obtained demonstrate impaired PMN phagocytic functions and CL response in diabetic patients. These findings suggest inhibitory effects of elevated glucose concentrations on PMNs, a possible role of protein glycosylation for impairing PMN function, thus contributing in part to altered host defense.     

Chemiluminescence of Human and Canine Polymorphonuclear Leukocytes in the Absence of Phagocytosis

Polymorphonuclear leukocytes (PMNs) have increased oxidative metabolism during phagocytosis and emit light (chemiluminescence, CL) as a result of metabolic activation. The present study examined PMN CL in the absence of phagocytosis using sodium fluoride (NaF), a nonparticulate agent and known stimulator of cellular oxidative metabolism. Normal human and canine PMNs were assayed in a CL spectrometer which permitted continuous sample mixing and constant temperature regulation during CL measurement. PMNs treated with 20 mM NaF demonstrated maximum CL responses of 10,000-20,000 cpm above background, 13-17 min after addition of NaF at 37 degrees C. Temperature regulation of reaction mixtures was found to be a critical factor in assaying PMN CL responses to NaF, because a small decrease in temperature (i.e. 1.5 degrees C) substantially depressed and delayed the CL response. Superoxide anion production correlated closely with CL responses in NaF-treated human PMNs. CL responses were completely suppressed in the presence of the oxidative metabolic inhibitors, iodoacetamide, and N-ethylmalemide; and were partially suppressed in the presence of either superoxide dismutase or sodium azide.CL responses of NaF-treated PMNs were significantly lower than responses generated by PMNs phagocytizing opsonized yeast. When NaF was evaluated for its effect on light generation from a singlet oxygen dependent CL reaction, it was found that NaF did not quench singlet oxygen light. This study demonstrates that PMN CL can occur in the absence of phagocytosis, and it proposes that a nonphagocytic PMN CL assay may be useful in evaluating leukocyte metabolic defects.     

Omega-3 fatty acids suppress the enhanced production of 5-Iipoxygenase products from polymorph neutrophil granulocytes in cystic fibrosis

Abstract. Pulmonary damage in cystic br osis (CF) is associated with chronic inflammation mediated in part by proinflammatory 5-lipoxygenase products (5-LOP, leukotrienes and 5-hydroxyeicosatetraenoic acid) from polymorph neutrophil granulocytes (PMN). The authors studied 5-LOP formation of PMN from CF patients and in vitro effects of added eicosapentae-noic acid (EPA) and fish oil. Circulating PMN were isolated from 10 CF patients without acute infections and 10 control persons of the same age (4–20 years). Total 5-LOP liberation from PMN of CF patients was significantly increased over controls after incubation with the calcium ionophore A23 (1 μmol L^-1) without arachidonic acid (AA) (380 ±24 vs. 294±28pmol mL^-1) and with 10μmolL^-1 AA (1303±104 vs. 1015 ± 104 pmolmL^-1), and there were nonsignificant trends to high values after incubation with 5μmolL^-1 platelet activating factor (PAF, 134% of controls) and 1 μmol L^-1 formyl-methionyl-leucyl-phenylalanine (FMLP, 125%). The addition of 100 mu;g mL^-1 fish oil to PMN of CF patients challenged with A23 completely suppressed synthesis of proinflammatory 5-LOP of the 4-series, while inactive 5-LOP metabolites of the 5-series were produced. Added EPA (10 μ molL^-1) also suppressed 4-series 5-LOP and significantly reduced leukotriene B₄ concentration by 48% from 39.9 ±3.2 to 20.6 ± 11.4 pmol L^-1 again with a concomittant increase of inactive 5-series metabolites. The authors conclude that the turnover of endogenous and exogenous AA is enhanced in CF, possibly due to stimulated phospho-lipase A₂ activity. The relatively small effect of the receptor dependent stimuli PAF and FMLP may be caused by a down-regulation of PMN receptors in CF. Supplementation of long-chain ω-3-fatty acids may be beneficial for reducing excessive inflammation in CF patients and should be further evaluated.     

Tolerance to endotoxin-induced expression of the interleukin-1 beta gene in blood neutrophils of humans with the sepsis syndrome.

The induction of genes of host cells stimulated by microbial products such as endotoxin and the tolerance of cells to endotoxin excitation play critical roles in the pathogenesis of microbial-induced acute disseminated inflammation with multiorgan failure (the sepsis syndrome). One gene that is induced in phagocytic cells by endotoxin and that appears to play an essential role in the pathogenesis of the sepsis syndrome is IL-1 beta. We report here that blood neutrophils (PMN) of patients with the sepsis syndrome (sepsis PMN) are consistently tolerant to endotoxin-induced expression of the IL-1 beta gene, as determined by decreased synthesis of the IL-1 beta protein and reductions in IL-1 beta mRNA. This down-regulation of the IL-1 beta gene in sepsis PMN occurs concomitant with an upregulation in the constitutive expression of the type 2 IL-1 receptor (IL-1R2). These phenotypic changes do not persist in PMN of patients recovering from the sepsis syndrome. Tolerance has stimulus and response specificity since sepsis PMN tolerant to endotoxin can respond normally to Staphylococcus aureus stimulation of IL-1 beta production and they normally secrete elastase. Uninfected patients with severe trauma or shock from causes are not tolerant to endotoxin and tolerance is not limited to patients infected with Gram-negative bacteria. The mechanism responsible for tolerance involves pretranslational events and is not due to loss of the CD14 surface protein, a receptor required for endotoxin induction of IL-1 beta in PMN. The physiological significance of the tolerance to endotoxin and increased expression of IL-1R2 on sepsis PMN is unknown, but may represent an attempt by the host to protect itself from the deleterious effects of disseminated inflammation.     

Enhanced phagocytic cell respiratory burst induced by spinal manipulation: potential role of substance P.

The effect of spinal manipulation on the respiratory burst of polymorphonuclear neutrophils (PMN) and monocytes from treated adults was measured by zymosan-stimulated chemiluminescence (CL). Peripheral blood was collected 15 min before and 15 min after treatment (sham manipulation, thoracic spine manipulation, or soft tissue manipulation), the cells were isolated, challenged with a standardized, opsonized luminol-containing suspension of zymosan, and monitored for CL. Plasma from two subsets of subjects was radioimmunoassayed for Substance P (SP). PMN were also preincubated with SP in vitro over the dose range 5 x 10(-12) M to 5 x 10(-8) M and the CL response monitored. The CL responses of both PMN and monocytes from subjects who received spinal manipulation were significantly higher after than before treatment, and significantly higher than the response in sham or soft-tissue treated subjects. Measurement of the force applied by sham and spinal manipulation suggested a force threshold for the enhancement of the CL response. Plasma levels of SP before and after treatment in sham treated subjects did not differ significantly; however, elevated plasma SP was observed in subjects after spinal manipulation. Preincubation of PMN with 1 x 10(-11) M, 5 x 10(-11) M or 1 x 10(-10) M SP in vitro primed PMN for an enhanced respiratory burst when the cells were subsequently challenged.     

Opsonophagocytic dysfunction in patients with liver cirrhosis and low responses to tumor necrosis factor-α and lipopolysaccharide in patients’ blood

To evaluate their defense level against bacterial infection of patients with liver cirrhosis, we compared the luminol-dependent chemiluminescence (CL) response of peripheral blood from 40 patients with that from 40 healthy volunteers. Small quantities of heparinized whole blood (100µl; final dilution, 1:10) were used for phagocytes, and CL was measured on addition of nonopsonized zymosan or Escherichia coli without special opsonization. Whole blood CL in cirrhotic patients was significantly lower than that in the healthy controls. The incidence of lower CL response in patients increased as disease stage advanced. Polymorphonuclear leukocytes (PMN) from cirrhotic patients exibited a slightly lower CL response than those from controls, but this was not statistically significant. In contrast, the CL response of monocytes in patients was significantly lower than that of controls. The opsonizing capacity of the patients sera and ascitic fluid was also decreased. In fact, the levels of opsonins such as complement in the patients sera and both immunoglobulins and complement in the ascitic fluids were found to be lower in cirrhotic patients. On the basis of these findings, defect of opsonophagocytic function seems to participate in the increased susceptibility to infection in cirrhotic patients. Furthermore, whole blood CL induced by nonopsonized zymosan at the onset of relatively severe bacterial infections such as sepsis, pneumonia, or spontaneous bacterial infection was less augmented in the blood of cirrhotic patients than that in noncirrhotic patients. To clarify the reason why whole blood exhibits a lower CL response in the acute phase of bacterial infections, we investigated the priming effects of lipopolysaccharide (LPS) or tumor necrosis factor- (TNF-), well-known CL activators, on the CL response of whole blood obtained from cirrhotic patients in comparison with that from healthy persons. The priming effects were significantly decreased in patients blood when compared with that of healthy persons. These low responses of patients blood to LPS or TNF- support our finding that phagocytes are not fully activated when gram-negative bacterial infections occur.     

Neutrophil chemotaxis and adherence in vitro and localization in vivo in rabbits with Staphylococcus aureus abscesses

Decreased neutrophil (PMN) function may contribute to an altered host defense system in hosts with bacterial abscesses but has not been well correlated to in vivo outcome. We have found that blood PMNs from rabbits with chronic (2-week) experimental Staphylococcus aureus abscesses have decreased chemotaxis in response to an S. aureus supernatant (370 +/- 130 microns migration vs 570 +/- 180 microns, p less than 0.05) and decreased adherence (11.5% +/- 13.2% vs 32.9% +/- 18.6%, p less than 0.005) compared with PMNs from animals with acute (24-hour) abscesses. No differences were found in chemokinesis, random migration, and chemotaxis in response to zymosan-activated serum. No plasma inhibitors of PMN chemotaxis or inhibitors of chemotaxins were found. Although animals with chronic abscesses had higher levels of circulating chemotaxins, in both groups of animals abscess chemotaxin levels were greater than the plasma chemotaxin level. Animals with a concomitant chronic abscess had less PMN influx into an acute abscess but also less bacterial growth within the abscess than animals without a concomitant chronic abscess. We conclude that rabbits with chronic staphylococcal abscesses have decreased chemotaxis and adherence measured in vitro and decreased PMN localization in vivo. In this model, these functions were not associated with increased bacterial proliferation in vivo.     

Increased expression of the interleukin 1 receptor on blood neutrophils of humans with the sepsis syndrome.

Because of the potential importance of interleukin 1 (IL-1) in modulating inflammation and the observations that human blood neutrophils (PMN) express IL-1 receptors (IL-1R) and synthesize IL-1 alpha and IL-1 beta, we studied the IL-1R on blood PMN from a group of patients with the sepsis syndrome. We report a marked enhancement in the sites per cell of IL-1R expressed on sepsis-PMN of 25 consecutively studied patients compared to 20 controls (patient mean = 9,329 +/- 2,212 SE; control mean = 716 +/- 42 SE, respectively). There was no demonstrable difference in the Kd of IL-1R on sepsis-PMN (approximately 1 nM) as determined by saturation curves of 125I-IL-1 alpha binding and the IL-1R on sepsis-PMN had an apparent Mr approximately 68,000, a value like that of normal PMN. Cytofluorographic analysis indicated that the sepsis-PMN phenotype is a single homogeneous population with respect to IL-1R expression. In contrast, expression of the membrane complement receptor CR3 is not increased on sepsis-PMN. Similar increases in expression of IL-1R were not observed in various other inflammatory processes, including acute disseminated inflammation and organ failure not caused by infection, acute infection without organ failure, and immunopathologies such as active systemic lupus erythematosus and rheumatoid arthritis. Enhanced expression of IL-1R was not related simply to the state of myeloid stimulation. Increased expression of IL-1R on normal PMN was induced in vitro by incubating cells with recombinant human granulocyte-macrophage/colony-stimulating factor for 18 h and this response was inhibited by cycloheximide, suggesting the possibility that de novo synthesis of IL-1R might occur in PMN during the sepsis syndrome.     

In Vitro Bactericidal Capacity of Human Polymorphonuclear Leukocytes: Diminished Activity in Chronic Granulomatous Disease of Childhood

Diminished bactericidal capacity was found to be characteristic of polymorphonuclear leukocytes (PMN) from five children with the clinical syndrome of granulomatous disease of childhood. The PMN from these children demonstrated nearly normal phagocytic capacity, and the majority of viable bacteria, after 2 hours of incubation in the phagocytosis system, were found associated with leukocytes.The morphology of the unstimulated polymorphonuclear leukocytes from patients with chronic granulomatous disease was similar to those from normal persons of similar ages by light and electron microscopy. In addition, the total lysozyme and phagocytin activity of leukocyte extracts from these patients was similar to those from equal numbers of leukocytes from controls.A striking difference in the cytoplasmic response after phagocytosis characterized the PMN of the patients with granulomatous disease. Whereas degranulation, vacuole formation, and rapid bacterial digestion were the rule in the PMN from controls, little degranulation and persistence of intact bacteria in the cytoplasm characterized disease.The deficiency of bactericidal capacity and the minimal degranulation after active phagocytosis by the PMN of these children with an inherited syndrome suggest that separate metabolic processes are involved in phagocytosis and in intracellular digestion. Continuing study of the metabolic function of leukocytes from these children should provide an opportunity for increased understanding of the metabolic basis for degranulation and intracellular digestion in phagocytic cells.     

健康妊娠和子痫前期患者血浆中血栓炎症表达谱差异分析

摘要:目的：观察正常妊娠过程和子痫前期（PE）血栓炎症性反应差异，为PE的早期诊断和预防策略改进提供工作基础。 方法：定制抗体芯片（覆盖大量细胞因子、止血相关蛋白质等）检测健康育龄女性、健康妊娠女性和子痫前期患者血浆，分析各组间差异蛋白质特征。 结果：健康妊娠组和健康育龄组有37种蛋白质水平差异有统计学意义，相对于健康育龄组，健康妊娠组有解整合素-金属蛋白酶12、趋化因子CCL2等16种蛋白质水平升高，粒-单细胞集落刺激因子（GM-CSF）和载脂蛋白F等21种水平降低；PE组和健康妊娠组有27种蛋白质水平差异存在统计学意义，相对于健康妊娠组，PE组有GM-CSF和血管内皮生长因子受体2（VEGFR2）等16种水平升高，肿瘤坏死因子相关凋亡诱导配体、干扰素Ω1等11种水平降低。进一步综合分析健康育龄组、健康妊娠组和PE组血浆蛋白质发现，PE患者血浆蛋白质出现更复杂的变化，更多参与炎症和免疫反应的细胞因子和急性期反应蛋白水平升高，更多控制炎症反应的细胞因子水平降低，促进血栓形成和参与补体反应的蛋白质水平升高，肾素水平降低以及VEGFR2水平升高。 结论：PE存在着比与健康妊娠更严重的炎症反应、止血和血管内皮系统失衡，提示研究PE的血栓炎症反应将有助于改进PE的诊断和预防策略。     

中性粒细胞凋亡调控基因表达异常在全身炎症反应综合征中的作用

目的观察全身炎症反应综合征（SIRS）时中性粒细胞（PMN）凋亡的异常变化及其凋亡调控基因的表达情况，评价其临床意义。方法8例SIRS患者（均为急性胰腺炎患者）作为SIRS组。6名健康献血者作为正常对照组。分别观察两组外周血PMN凋亡率、凋亡调控基因Fas／FasL和凋亡信号转导分子天冬氨酸特异性半胱氨酸蛋白酶-3（caspase-3）及血清白细胞介素-6（IL-6）、IL8的水平。结果SIRS组外周血血清IL-6和IL-8水平均明显高于正常对照组（P均＜0．01）。SIRS组患者外周血PMN细胞凋亡率较正常对照组明显减少（P＜0．01）；两组PMN在体外培养24h后，用蛋白质免疫印迹法（Western blotting）没有检测到FasL表达；SIRS组患者外周血PMN的Fas、caspase-3表达水平与正常对照组比较明显降低（P均＜0．01）。结论SIRS患者存在PMN的凋亡异常和Fas、caspase-3表达水平下调，PMN凋亡延迟在SIRS的发生发展中有着重要意义。     

Sonography of acute appendicitis in pregnancy

Background: Clinical evaluation of acute appendicitis is difficult in pregnant patients. Delay in diagnosis is associated with increased fetal mortality. The purpose of our study was to assess the value of sonography in the diagnosis of acute appendicitis in pregnant women. Methods: We obtained sonograms in 22 pregnant women suspected of acute appendicitis. All sonograms were performed using graded-compression to detect an enlarged appendix. The sonographic criteria for acute appendicitis were detection of a noncompressible blindended and tubular multilayered structure of maximal diameter greater than 6 mm. Results: The sonographic findings were correlated with surgical findings in seven cases and clinical follow-up in 15 cases. Acute appendicitis was diagnosed by sonography in three of 22 patients, and in all but one was confirmed by surgical and pathologic findings. In the remaining 19 patients, 15 improved on clinical follow-up; three were shown to have a normal appendix at surgery and one had focal acute inflammation at the tip of the appendix. Conclusions: Our experience suggests that graded-compression sonography is a useful procedure in pregnant patients suspected of acute appendicitis and has a similar accuracy as in nonpregnant women, especially in the first and second trimester.     

Cosmetic liposuction causes only transient elevation of acute inflammatory response and does not advance to oxidative and nitrosative stress

Cosmetic liposuction is a surgical procedure performed on normal nonobese subjects to remove unwanted fat. We are interested to know whether the impact of acute inflammatory response induced by liposuction differs from that of chronic inflammation and whether acute inflammatory response will also advance further and cause oxidative and nitrosative stress leading to various clinical complications. In our investigation we monitored 15 nonobese women prior to liposuction, and one day and one month after the surgery with multiple markers associated with chronic inflammation and oxidative stress. Our results indicate that liposuction causes only a transient elevation of acute inflammatory markers such as interleukin-6 (IL-6), high sensitive C-reactive protein (hCRP), and serum amyloid A (SAA), and a transient decrease of nitric oxide (NO). Apparently the impact of liposuction for normal subjects did not advance beyond acute inflammatory response; there was little change in the levels of markers corresponding to downstream events of chronic systemic inflammation such as adhesion molecules, urinary microalbumin (uMA), homocysteine (Hcy), uric acid (UA), and markers of oxidative stress, including urinary 8-hydroxydeoxyguanosine (8-OhdG) and 3-nitrotyrosine (3NT). It appears that the acute inflammatory response of cosmetic liposuction does not lead to impaired renal function and oxidative and nitrosative damage, which are frequently associated with chronic inflammation.     

Dialysis in Older Patients

Older persons with chronic uremia tolerate hemodialysis or a renal transplant as well as younger patients. However, this is not true in acute renal failure. One of the most distressing problems during hemodialysis in elderly patients with acute uremia is aspiration pneumonitis with respiratory arrest. Most problems with dialysis for patients past age 50 are related to illnesses more common in older persons.     

The effect of psychological stress on neutrophil superoxide release

Stress has long been suggested to exacerbate symptom expression in people with chronic inflammatory disorders. The release of oxidative metabolites from activated PMN plays a significant role in the pathophysiology of inflammation. Thus, we examined the effects of psychological stress on release of superoxide anions from PMN of rats with or without an inflammation induced by injection of shellfish glycogen (SFG). Psychological stress was found to significantly increase PMN superoxide release in both healthy and SFG-injected animals. Total amounts of superoxide release were similar between the two groups, suggesting that PMN from animals with a mild inflammatory condition were not more susceptible to the effects of stress than PMN from healthy animals. However, this study should be repeated using an animal model of chronic inflammation, such as airway hyperactivity or rheumatoid arthritis.     

经阴道超声联合胎儿纤维连接蛋白预测自发性早产的临床价值

  目的  分析经阴道超声测量子宫宫颈前角（ACA）、宫颈长度（CL）联合胎儿纤维连接蛋白（fFN）预测自发性早产（SPB）的临床价值。  方法  选取2019年6月~2022年6月我院收治的98例先兆早产孕妇为研究对象,根据是否发生SPB将其分为SPB组（n=33）和足月组（n=65）。采用单因素及Logistic多因素回归分析先兆早产孕妇发生SPB的风险因素。通过绘制ROC曲线评估ACA、CL及fFN对SPB的预测效能。  结果  经单因素分析,两组孕前BMI、胎膜早破、宫内感染、羊水过多、妊娠期糖尿病情况及ACA、CL、fFN水平的差异有统计学意义（P < 0.05）。经Logistic多因素回归分析,胎膜早破、ACA、fFN是先兆早产孕妇发生SPB的风险因素（OR>1,P < 0.05）,孕前BMI、CL是先兆早产孕妇发生SPB的保护因素（OR < 1,P < 0.05）。ROC曲线显示,当ACA≥ 116.500°时,预测先兆早产孕妇发生SPB的AUC为0.630,敏感度为48.5%,特异性为69.2%。当CL≤25.000 mm时,AUC为0.667,敏感度为54.5%,特异性为73.8%。当fFN≥96.155 μg/L时,AUC为0.652,敏感度为60.6%,特异性为69.2%。三者联合预测的AUC为0.740,敏感度为72.7%,特异性为75.4%。  结论  经阴道超声测量ACA、CL及fFN水平均对预测先兆早产孕妇发生SPB具有一定预测价值,且三者联合预测效能更佳。