RNA原位杂交法检测灌胃接种弓形虫速殖子小鼠体内虫体的早期动态分布

目的观察经灌胃接种弓形虫RH株速殖子后,虫体在小鼠体内的早期动态分布。方法弓形虫RH株速殖子经灌胃接种BALB/c小鼠20只(2×104/只),用RNA原位杂交法观察感染后1、2、4、6和8d小鼠的肠系膜淋巴结(MLN)、肝、脾、肺和脑组织内速殖子的数量及分布趋势。同时设PBS空白对照组(5只)。结果感染后1d,在MLN、肝和脾组织内均检测到速殖子,分别于感染后4d和6d在肺和脑组织内检测到速殖子。感染后6～8d,各组织间虫荷差异均有统计学意义(P值均0.05),组织内虫荷依次为MLN肝脾肺脑,各组织内虫体数量呈时间依赖性。结论弓形虫RH株速殖子经灌胃接种后,首先侵入MLN、肝和脾,其次为肺,最后为脑,且虫体在MLN内增殖较快。     

Changes in hemopoiesis of mice of the C3H strain following transplantation of Gardner lymphosarcoma and infection with LDH-virus. I. Circulating blood

The values of red and white blood count, of spleen and liver weight were determined in mice of the C3H strain after transplantation of Gardner solid lymphosarcoma contaminated with LDH-virus and after infection of LDH-virus, and compared with those found in normal intact mice. Special attention was devoted to early post-transplantation period and the final stage of tumor growth. The second day after infection of mice with LDH-virus, leukopenia with marked lymphopenia was observed, together with a reduced number of reticulocytes and spleen enlargement. The same changes became more pronounced in tumorous mice on the second posttransplantation day. The changes--with the exception of spleen enlargement--following LDH-virus infection became normalized within the period of the final stage of tumor growth. Contrarily, in mice with tumors in the final stage of the disease besides spleen enlargement also the reduced erythrocyte counts, leukopenia with pronounced lymphopenia and thrombocytopenia were found.     

Altered protein hypothesis of mammalian ageing processed-I. Thermal stability of glucose-6-phosphate dehydrogenase in C57BL/6J mouse tissue.

Relative enzymatic activity and thermal stability were determined for glucose-6-phosphate dehydrogenase obtained from five tissues of C57BL/6J female mice as a function of age. Tissues studied were brain, spleen, liver, kidney and lung, and measurements were taken up to three-quarters the maximum lifespan (young, 170 days; old, 750 days). Relative enzyme activity increased in all organs by approximately 60 per cent on either an activity per organ or per weight basis. Per cent thermolabile enzyme increased from approximately 0–5 per cent for young to 10–15 per cent for old animals. A starvation period of 40 hr for old animals resulted in lowering the per cent thermolabile G-6-PD for brain, spleen and liver tissues (0–5 per cent thermolabile protein remaining). These results are consistent with the altered protein hypothesis as an important primary ageing process and of protein degradation as a possible effective means to reduce altered proteins in vivo.     

田鼠巴贝虫感染BALB/c小鼠血细胞动态变化

目的 观察小鼠感染田鼠巴贝虫（Babesia microti）后体重、脾脏及血液细胞的变化情况。方法 取田鼠巴贝虫感染种鼠外周血（虫密度为20%）,腹腔接种6周龄健康BALB/c小鼠,100 μL/只,并设立健康小鼠对照组。感染组小鼠于感染后0～28 d隔日尾尖采血,涂薄血片,吉氏染色后油镜下观察田鼠巴贝虫增殖情况,并分别于感染后0、7、14、21、28 d测定小鼠体重、脾重,采用全自动血细胞分析仪分析小鼠血细胞。结果 小鼠在感染后第1天即可在外周血中查见田鼠巴贝虫虫体,第7天染虫率最高（55%）,随后感染率逐渐下降,至第28天外周血虫体镜检阴性,进入隐性感染阶段。小鼠于感染后第7天体重降至最低,随后逐渐恢复;脾脏重量在感染后第14天最重,后逐渐降低,但至第28天脾重仍高于正常组。全血细胞分析发现,感染组小鼠白细胞数量及淋巴细胞、嗜酸性粒细胞比例无明显变化,波动范围在正常小鼠参考值范围内。感染组小鼠红细胞计数、血红蛋白含量及血小板计数在感染后虫密度高峰期降至最低,后随着虫密度降低而逐渐恢复至正常水平。结论 田鼠巴贝虫感染可引起小鼠体重下降、脾脏增重、红细胞及血小板数量降低,全血细胞分析仪对巴贝虫病诊断具有参考价值。     

Changing response of Plasmodium falciparum to chloroquine in West Bengal during 1980-1988

A total of 314 cases of Plasmodium falciparum malaria studied during 1980-88 in nine times monitoring revealed three RIII foci i.e. two in Jalpaiguri and one in Purulia districts. The studies showed a parasite clearance of 40 per cent and 32 per cent of P. falciparum cases within seventh day in Purulia and Jalpaiguri districts respectively, with a dosage of 25 mg per kg body weight, spread over three days in divided doses. Increase in transmission potential and prolonged drug pressure with single drug have been noted in association with development of resistance. Malaria parasite clearance time (MPCT) value of sensitive and resistant cases reach parallelism and malaria parasite recrudescence time (MPRT) value starts declining, giving an indication of stabilisation of genetic change in the parasite.     

Adrenalectomy reduces but does not reverse obesity in ob/ob mice

Bilateral adrenalectomy (ADX) of 4-month-old ob/ob mice led to reduced rates of body weight gain, a complete cessation of fat deposition and increased percentage carcass protein and ash during a 2-month observation period after surgery. However, ADX obese mice were still heavier and had more body fat and lower concentrations of carcass protein and ash than intact sex-matched littermate lean mice at the end of the experiment. When adrenalectomy was performed in younger obese mice before the syndrome was fully expressed (23 +/- 2 days of age), body weight gain was reduced by 40 per cent and fat deposition by 50 per cent during the next 3.5 months, but each was still greater than that of littermate lean mice. Despite the lower rate of weight gain after adrenalectomy, the skeletal and lean body growth of the early ADX obese mice equalled that of both obese and lean mice fed ad libitum. When the carcass composition of early ADX obese mice was compared with that of intact obese mice which were calorically restricted to the same rate of body weight gain, the ADX group had significantly less carcass fat (28 per cent) and more protein (50 per cent) and ash (20 per cent) than the dieted obese mice. In both experiments adrenalectomy led to reduced circulating immunoreactive insulin levels, although hyperinsulinemia persisted. The present results show that adrenalectomy is an effective tool for ameliorating the severity of many aspects of the ob/ob syndrome, particularly when compared with caloric restriction, but the procedure does not entirely reverse the deranged metabolism or abnormal carcass composition of these mice.     

IL-10 is not required to prevent immune hyperactivity during memory responses to Toxoplasma gondii

Primary infection of IL-10 knockout (KO) mice with the protozoan parasite Toxoplasma gondii leads to a CD4(+)-T-cell dependent shock-like reaction with high systemic levels of IL-12 and IFN-gamma, severe liver pathology and death of mice. In the present study, this immune-mediated pathology was prevented by treatment of IL-10 KO mice with the anti-parasitic drug sulfadiazine, allowing these mice to progress to the chronic phase of infection. To address the role of endogenous IL-10 in the regulation of secondary immune responses to T. gondii, IL-10 KO mice were infected with the avirulent Me49 strain of this parasite, treated with sulfadiazine for 2 weeks starting at day 3 p.i., and were rechallenged 6 weeks p.i. with RH, a highly virulent strain of T. gondii. In these studies, chronically infected IL-10 KO mice survived secondary infection with RH and controlled parasite load. Although serum levels of IL-12 and IFN-gamma were higher in IL-10 KO mice than in wild type (WT) mice 8 days after RH rechallenge, these levels were well controlled in the absence of endogenous IL-10, suggesting that IL-10 is not required to down-regulate cytokine production during the memory response. Antigen-specific ex vivo recall responses further revealed that splenocytes from chronically infected WT and IL-10 KO mice responded to parasite antigen with similar production of IL-12 and IFN-gamma, and there was also no significant difference in ex vivo production of these cytokines by splenocytes in response to parasite antigen 7 days after secondary infection with T. gondii. Furthermore, IL-10 KO mice immunized with the Ts-4 vaccine-strain of T. gondii were protected when rechallenged with the virulent RH strain. Together, these studies demonstrate that the inhibitory effect of IL-10, which is required to prevent immune-mediated pathology during primary infection, is not required to prevent immune hyperactivity during a secondary response to T. gondii, and a highly effective memory response is generated in the absence of endogenous IL-10.     

Effect of low frequency low energy pulsing electromagnetic fields on mice injected with cyclophosphamide

C3H mice have been used to investigate the effect of a combination of cyclophosphamide (CY) and electromagnetic fields (PEMF). Mice were injected i.p. with a single dose of 200 mg/kg body weight of CY and then exposed to PEMF 24 h per day. In an initial series of experiments immediately after CY injection mice were exposed to PEMF until sacrifice. WBC counts in the peripheral blood demonstrated a quicker decline in WBC at days 1 and 2 in mice exposed to PEMF. Groups of mice were sacrificed at days 1, 4, 6, 8, and 10 after CY injection. In mice exposed to PEMF the spleen weight was less than in controls at days 6, 8, and 10. Autoradiographic studies demonstrated that the labeling index of bone marrow smears did not significantly differ between controls and experimental mice exposed to PEMF, whereas the spleen labeling index proved to be higher among control mice versus mice exposed to PEMF at day 6, and higher among mice exposed to PEMF versus controls at day 8. In a second series of experiments mice were exposed to PEMF only over the 24 h following CY injection. We found that the spleens of mice exposed to PEMF weighed less than those of controls at days 6 and 8. The labeling index of bone marrow did evidence a slight decrease among mice exposed to PEMF at days 8 and 10 after CY injection versus control mice. The spleen labeling index proved to be lower in experimental mice exposed to PEMF than in controls at days 4, 6, and 8. Mice were then injected with CY, half were exposed to PEMF, and 24 h later bone marrow was recovered from both groups of animals. The same number of bone marrow cells was injected via the tail vein into recipient mice irradiated to 8.5 Gy. The grafting efficiency of the bone marrow was evaluated by examining the number of spleen colonies and the spleen and bone marrow labeling indices at day 8; all parameters proved to be significantly lower among mice grafted with the bone marrow of mice injected with CY and exposed to PEMF than among controls injected with CY only. Finally, we found th at the effect of PEMF is evident only if mice are exposed during the 24 h following CY injection. The data reported here indicates that PEMF exposure after CY injection increases the damage induced in mice by CY.     

Comparison of immune responses in mice infected with different strains of Strongyloides venezuelensis

In human hosts and in murine models, the immune response to Strongyloides spp. is Th2 type. In addition, the profile of the host immune response follows various symptoms induced by Strongyloides spp. In the present study, we demonstrated that the L2 and L49 strains of Strongyloides venezuelensis obtained from Bolomys lasiurus and Nectomys squamipes induced significant and similar increases in eosinophil/mononuclear cell counts in the blood, peritoneal cavity fluid and bronchoalveolar lavage fluid when compared with uninfected mice. However, in the first 3 days of infection, IL-4, IL-5 and IFN-gamma levels were higher in the lungs of mice infected with the L2 strain, which also presented greater production of IgG and IgG1 than did mice infected with the L49 strain. The higher antibody and cytokine levels induced by the L2 strain correlated with a decrease in the number of female parasites recovered in the faeces of mice on post-infection day 7. The results demonstrate that the L2 strain was a more potent stimulant of the humoral immune response, which can result in more efficient antibody-dependent cell-mediated cytotoxicity, a mechanism involved in eosinophil activation and parasite elimination. Further studies are needed in order to elucidate the molecular differences among parasites.     

First attempt to produce experimental Campylobacter concisus infection in mice

AIM： TO infect mice with atypical Campylobacter concisus （C. concisus） for the first time. METHODS： Three separate experiments were conducted in order to screen the ability of five clinical C. concisus isolates of intestinal origin and the ATCC 33237 type strain of oral origin to colonize and produce infection in immunocompetent BALB/cA mice. The majority of the BALB/cA mice were treated with cyclophosphamide prior to C. concisus inoculation to suppress immune functions. Inoculation of C. conc/sus was performed by the gastric route. RESULTS： C. concisus was isolated from the liver, ileum and jejunum of cyclophosphamide-treated mice in the first experiment. No C. concisus strains were isolated in the two subsequent experiments. Mice infected with C. concisus showed a significant loss of body weight from day two through to day five of infection but this decreased at the end of the first week. Histopathological examination did not consistently find signs of inflammation in the gut, but occasionally microabscesses were found in the liver of infected animals. CONCLUSION： Transient colonization with C. concisus was observed in mice with loss of body weight. Future studies should concentrate on the first few days after inoculation and in other strains of mice.     

Nitric oxide and reactive nitrogen intermediates during lethal and nonlethal strains of murine malaria

The virulence of Plasmodia depends partly on the strain of parasite and partly on the host. In this study, Plasmodium berghei N/13/1A/4/203 caused the death of mice, whereas Plasmodium chabaudi chabaudi AS was not lethal. Current opinion is that nitric oxide (NO) and other reactive nitrogen intermediates (RNI) are produced in several host organs during malaria to resist infection or produce tissue damage. NO and RNI production in blood or plasma, brain, liver and spleen in MF1 mice was investigated during P. berghei and P. c. chabaudi infection, in order to help determine whether changes in NO production are beneficial or detrimental to the host in vivo. NO production was measured both directly and indirectly as nitrites and nitrates, to represent RNI. No changes in blood NO were detected in P. berghei infected mice, but increases were observed in brain, liver and spleen. In P. c. chabaudi infected mice, rises in NO concentration were observed in blood and spleen, whereas a decline in liver NO was seen, but there were no changes in brain. Liver contained the highest concentration of RNI, but increasing concentrations were seen in both plasma and spleen in both P. berghei and P. c. chabaudi infected mice. These results show that NO and RNI production alters during murine malaria. The changes depend upon the tissue, the day of infection, the degree of parasitaemia, the strain of Plasmodia and the method of measuring NO biosynthesis. Lethal P. berghei induced NO production in the mid and late stages of infection in mice when parasitaemia was high, whereas in nonlethal P. c. chabaudi infection, NO production was increased in the early and late stages when parasitaemia was low. These data are consistent with a role for NO in the protection of the MF1 mouse against Plasmodia. Failure to clear the parasite is associated with evidence of increased NO production in brain and liver, which may contribute to the pathology of malaria, but this hypothesis requires confirmation from other experimental approaches.     

Fialuridine accumulates in DNA of dogs, monkeys, and rats following long-term oral administration.

Accumulation of the antiviral nucleoside analogue fialuridine (FIAU; 1-(2'-deoxy-2'-fluoro-beta-D-arab-inofuranosyl-5-iodouracil) in genomic DNA was examined with a modified version of a recently developed RIA for FIAU. DNA was obtained from tissues of dogs administered FIAU at 0, 1, 2, or 3 mg/kg of body weight per day for 90 days, monkeys administered FIAU at 0 or 25 mg/kg per day for 30 days, and rats administered FIAU at 0, 255, or 510 mg/kg per day for 70 days. FIAU incorporation was observed in all species. In the rat, FIAU was incorporated into DNA of all tissues examined, with highest concentrations in the liver followed by jejunum, spleen, and heart. FIAU was also incorporated into sperm DNA. Incorporation rates were as high as 11,000 pmol of FIAU per mumol of thymidine or 1 FIAU molecule per 90 thymidine molecules. In dogs and rats, the extent of incorporation was dose-dependent. Across species, FIAU concentrations in DNA were not singly dependent on the total dose administered but also may have been dependent on the duration of exposure. These studies show that FIAU accumulates to high concentrations in genomic DNA of liver as well as other tissues during chronic oral administration and suggest that net accumulation of FIAU in DNA may be a critical step in FIAU-induced toxicity.     

The detection of normal hidden stem cells during the development of leukemia: assays with PGK isozyme

We evaluated the changes in the number of normal spleen colony-forming units (CFU-S) in the spleen and the bone marrow of C3H/He mice during the development of leukemia following the injection of the murine leukemia cell line, MK-8057, MK-8057 cells, originating in C3H/He PGK-1b mice, were injected into syngeneic C3H/He PGK-1a mice so that phosphoglycerate kinase (PGK) isozymes could be used to distinguish leukemic spleen colonies from normal colonies when cells from the spleen or bone marrow of the recipients were reinjected into lethally irradiated mice. Leukemic cells showed a logarithmic increase in the recipient mice and had replaced the bone marrow and the spleen completely by days 6-8; the mice started to die of leukemia after day 11. However, colonies examined from normal stem cells still comprised 60% of the total number of spleen colonies on day 6, 45% on day 8, and 20% on day 10. Furthermore, when the numbers of normal CFU-S were calculated as numbers per spleen, we found that they increased exponentially to a level 100 times higher than the normal level 10 days after injection of MK-8057 cells.     

Evaluation of biologic activity of ferric chloride-treated endotoxin in mice.

Endotoxin (lipopolysaccharide, LPS) treated with ferric chloride was tested for its potential as a non-toxic agent for enhancement of non-specific host resistance. A 1 mg dose of untreated endotoxin, injected i.p. into mice, resulted in 100 per cent mortality, whereas the same amount of chemically-treated endotoxin resulted in less than 35 per cent lethality. The radio-protective potential of the treated endotoxin was similar to that of untreated endotoxin, as 70 per cent of each group of mice tested with either substance survived a dose of 850 rad x-ray. Irradiated mice, challenged 8 days after 850 rad x-irradiation, died when injected with 25 mug of either untreated or treated endotoxin. Antibiotic decontamination of the intestinal tract of host animals reduced the possibility of toxicity from endogenous endotoxin after challenge. This treatment resulted in 100 per cent survival from a 25 mug challenge at 8 days post-irradiation. The ferric chloride-treated proved to be a more effective B-lymphocyte mitogen. At a dose of 100 mug, treated endotoxin resulted in a 50 per cent greater mitogenic stimulation of B-lymphocytes as compared with that found after exposure to untreated endotoxin. Several lines of evidence support the contention that tolerance to untreated endotoxin was induced by repeated injections of either endotoxin preparation 1) 100 per cent of all endotoxin-tolerant mice survived a 1 mg challenge dose of untreated endotoxin, 2) there was a reduced mitotic response of splenic B-lymphocytes after re-exposure with untreated endotoxin as compared with that observed for cells derived from saline-treated mice, and 3) all antibiotic decontaminated mice engrafted with spleen cells from mice made tolerant to either endotoxin preparation survive graft-versus-host disease. In conclusion, based on survival data from normal mice, ferric chloride-treated endotoxin is safer to use than normal endotoxin. Also, treated endotoxin can elicit biologic responses similar in magnitude to those found after injection of mice with untreated endotoxin.     

Changes in lymphoid organs of Ames dwarf mice after treatment with growth hormone, prolactin or ectopic pituitary transplants.

This study was performed to obtain more insight into the roles of PRL and GH in the control of immune functions in hereditary dwarf mice characterized by severe immunodeficiency. Adult female Ames dwarf mice (df/df) were injected daily for 10 days with ovine PRL (oPRL), bovine GH (bGH), oPRL+bGH or were implanted with a normal pituitary under the kidney capsule for 5 days. Only the treatment with bGH resulted in significant increases in the gain of body weight, and in absolute and relative thymus and spleen weights. Treatment with oPRL alone did not affect body weight gain or thymus and spleen weights. Treatment with oPRL+bGH produced a significant increase in the gain of body weight and in absolute and relative spleen weight but these effects were smaller than those measured in dwarf mice treated with bGH alone. Only bGH therapy resulted in extensive recovery of the absolute number of lymphocytes in the thymus and spleen of dwarf mice, with the values in treated dwarf mice not significantly different from those found in normal non-dwarf females. However, when these values were corrected for body weight, both the splenic and the thymic indices exceeded the values found in normal mice. The absolute numbers of lymphocytes in the spleen were also increased by oPRL+bGH treatment, but did not reach the values found in normal mice; however, the splenic index exceeded the values found in normal animals. Surprisingly, the absolute and relative numbers of lymphocytes found in the thymus of dwarf mice under oPRL+bGH therapy were indistinguishable from those found in oPRL or vehicle treated dwarf mice.(ABSTRACT TRUNCATED AT 250 WORDS)     

Waterborne typhoid fever in Dade County, Florida. Clinical and therapeutic evaluation of 105 bacteremic patients.

An extensive outbreak of waterborne typhoid fever occurred in 1973 at a migrant labor camp in Dade County, Florida. Blood cultures from 105 of the 188 patients with proved or presumptive cases of typhoid fever grew Salmonella typhi. The clinical and laboratory findings in these patients were reviewed. Fever, usually with temperatures above 38.8 degrees C and of the sustained type, was a primary manifestation of disease, although a majority of the patients also complained of headache and gastroenteric symptoms. Hepatic or splenic enlargement was present in 52 per cent and 42 per cent, respectively, whereas rose spots were detected in only 13 per cent. The total leukocyte count was normal in 74 per cent, but serum levels of liver and muscle enzymes were frequently elevated. Gastrointestinal, pulmonary and neurologic complications were infrequent; circulatory failure was not observed. Defervescence in response to antibiotic therapy was variable; however, the median response among 68 patients who received chloramphenicol was two days less than that in 34 patients treated with ampicillin. There was one possible treatment failure with ampicillin. The relapse rate of 10 per cent in chloramphenicol-treated patients was not significantly greater than the 3 per cent rate among those treated with ampicillin. Serologic studies for typhoid fever were of limited diagnostic value since the titer of agglutinins was 1:160 or higher in 49 per cent of the serums obtained before treatment, and a fourfold rise in titer occurred in only 24 per cent of 57 patients studied. The serologic response to chloramphenicol treatment did not differ from that to ampicillin.     

Animal model for immune dysfunction associated with adenosine deaminase deficiency.

An in vivo murine model for immunodeficiency of both B and T cells is produced by continuous intraperitoneal infusion of 2'-deoxycoformycin (DCF), a specific tightly binding inhibitor of adenosine deaminase (ADase; adenosine aminohydrolase, EC 3.5.4.4). After DCF infusion, ADase of thymus, spleen, and lymph nodes was inhibited to varying degrees ranging from 57% to 100%. Immunodeficiency under these conditions was indicated by: (i) a striking decrease in lymphocyte response to the T-cell mitogens concanavalin A and phytohemagglutinin; (ii) an impairment of delayed hypersensitivity measured by the footpad reaction; (iii) a decrease in antibody production measured in both in vivo and in vitro plaque-forming cell assay; (iv) a significant prolongation of mouse skin allograft survival after transplantation into the C57BL/6J (H-2b) strain of skin from BALB/c (H-2d) mice; and (v) a marked lymphopenia. Histological examination indicated lymphoid degeneration in the thymus, lymph nodes, and spleen with no alterations in other tissues including bone marrow, kidney, lung, gastrointestinal tract, and liver except for the occurrence of hepatitis. A decrease in the number of Thy-1-positive cells in both spleen and lymph nodes further supported the fact of cytotoxicity of DCF to T cells. Anorexia and weight loss were observed within 5 days of continuous DCF infusion at 0.4 mg/kg body weight per day. These data indicate that this method provides an experimental model for future studies on the biochemical mechanisms responsible for the genetically determined severe combined immunodeficiency disease in man.     

Kinetics of the nucleoside triphosphate hydrolase of Toxoplasma gondii in mice with acute and chronic toxoplasmosis

The kinetics of the nucleoside triphosphate hydrolase (NTPase) of Toxoplasma gondii was examined using an avidin-biotin sandwich-ELISA (ABS-ELISA) based on an anti-NTPase monoclonal antibody, 6C6. The RH and ME49 strains of the parasite were used to produce acute and chronic infections in mice, respectively. In the acute model, detectable serum concentrations of NTPase were observed from day 1 post-infection and gradually increased until the death of the mice. They were associated with parasitaemia (as estimated by bioassay). No anti-T. gondii antibody could be detected at any time. In the chronic model, in which 20 T. gondii ME49 cysts were given to each mouse per os, the NTPase concentration generally increased from day 3, peaked between days 7 and 14 and then declined. However, one of the four mice used still had a high serum concentration of NTPase on day 35. Again, detectable NTPase concentrations occurred when the mice had parasitaemias. Antibody to T. gondii was detected from day 7 (IgM) or 10 (IgG) and brain cysts were observed from day 14. Since detectable serum concentrations of NTPase appear to be associated with parasitaemia in both acute and chronic toxoplasmosis, the ABS-ELISA of the enzyme may make a useful diagnostic tool.     

Long-term changes of body weight in adult obese and non-obese men

In this study the long-term changes of body weight during adulthood in men obese as young adults are compared to those occurring in a random sample from the underlying population. Among 362,200 Danish draftees from 1943 to 1977, 1940 were obese (body mass index greater than or equal to 31 kg/m2). A random sample, comprising 0.5 per cent (1801), was drawn from the remaining population. In 1981-83, 4-40 years later, those living in the same region were invited to a health examination, which was attended by 964 (58 per cent) obese and 1134 (75 per cent) control subjects. In the obese group median change of body weight was 1.3 kg, and in the control group 8.3 kg. Weight change was positively correlated to duration of observation in both groups. Those with lowest body mass index at first examination tended to increase most, and those with highest body mass index tended to lose weight. However, the 5th to 95th percentiles of changes in body weight extended in the obese group from -24 to 29 kg, and in the control group from -2 to 25 kg. The range in weight change increased strikingly with increasing first body mass index exceeding 27 kg/m2. The study indicates that the greater the body mass index among young adult men, the less is the median change in body weight, but the greater is the variation of the body weight changes. These results suggest that the size of the fat mass is subject to intra-individual environmental influences that change over time.     

小鼠感染弓形虫Prugniaud株后的组织病理学变化

目的观察ICR小鼠感染Prugniaud株弓形虫后的症状和组织病理学动态变化。方法 46只ICR小鼠随机分为感染组(30只)和对照组(16只),感染组小鼠经腹腔注射弓形虫Prugniaud株包囊(10个/鼠,悬于0.5 ml PBS中),对照组小鼠注射等量PBS。每天观察小鼠发病情况,并于感染后第5、10、15、20、25、30、60和90天,分别处死感染组小鼠3只和对照组小鼠2只,取小鼠肝、脾、肺、肾、心和脑组织制作切片,HE染色和免疫组织化学检测。结果感染组小鼠于第6天开始出现食欲减退、耸毛、抖动和腹泻等症状,死亡率为20.0%。HE染色镜检发现第5天至20天,肝组织结构破坏,少数肝细胞水肿,气球样变和小灶性肝细胞坏死,肝窦扩张充血伴有炎症细胞浸润等;脾脏可见脾小体破坏、消失,脾窦扩张充血,红髓增宽白髓萎缩等。肺组织结构破坏,出现间质性肺炎等病理改变。感染第20天后上述组织病理变化逐渐减轻至恢复。脑组织从感染第10天起出现神经元变性、坏死,第15天~90天出现神经胶质结节、血管袖套现象和珠网膜下腔炎症细胞浸润等,并可见弓形虫包囊,第90天珠网膜下腔内见肉芽组织。免疫组织化学法检测结果显示,感染第5天内脏器...