甲亢患者服用131I治疗前后淋巴细胞SCE频率和染色体畸变率的研究

甲亢患者服用１３１Ｉ治疗前后淋巴细胞ＳＣＥ频率和染色体畸变率的研究詹喜焱代军胡绍表１甲亢患者服用１３１Ｉ前一天、服用１３１Ｉ后第６天和６个月ＳＣＥ频率和染色体畸变率的比较例数ＳＣＥ／细胞（ｘ±ｓ）染色体畸变率（％）（ｘ±ｓ）服用１３１Ｉ前１天６０４．...     

孕妇被动吸烟自身和子代SCE及对子代智商和身体健康素质影响的研究

本实验室随机选择被动吸烟孕妇及正常孕妇各３０例进行ＳＣＥ表达频率的研究,而且选择检测组中１５例服用叶酸试验治疗,对比值有显著差异。检测组ＳＣＥ表达频率为３．６％,对照组子代ＳＣＥ表达频率为２．８％;服用叶酸检测组ＳＣＥ表达频率为５．７％,未服用叶酸检测组ＳＣＥ表达频率为７．３％;研究数据提示被动吸烟可诱发ＳＣＥ表达频率增高,从而使染色体不稳定性增加,染色体畸变率增高。ＳＣＥ表达频率频繁的染色体及部位有２ｐ１１、３ｐ１４、９ｐ１２、１１ｐ１１、１６ｐ１１、２１ｐ１３、Ｘｐ２３。     

溴氰菊酯对白纹伊蚊（Aedesalbopictus）C6／36细胞株的细胞遗传学效应

本研究选择１０μｇ／ｍｌ、２０μｇ／ｍｌ、４０μｇ／ｍｌ浓度的溴氰菊酯处理白纹伊蚊Ｃ６／３６细胞，以ＭＭＣ作为阳性对照物，观察溴氰菊酯处理２４ｈ后对Ｃ６／３６细胞染色体畸变率和姐妹染色单体互换（ＳＣＥ）频率的影响。结果显示，三个浓度的溴氰菊酯对Ｃ６／３６细胞染色体畸变率均没有显著影响（Ｐ＜０．０５）；溴氰菊酯浓度在４０μｇ／ｍｌ时可诱导Ｃ６／３６细胞ＳＣＥ频率轻度增高（Ｐ＞０．０５），而溴氰菊酯浓度在１０μｇ／ｍｌ、２０μｇ／ｍｌ时，对Ｃ６／３６细胞ＳＣＥ频率没有诱导作用。表明溴氰菊酯对Ｃ６／３６细胞的遗传学效应较弱     

孕妇被动吸烟自身和子代SCE及对子代智商和身体健康素质影 …

本实验室随机选择被动吸烟孕妇及正常孕妇各３０例进行ＳＣＥ表达频率的研究,而且选择检测组中１５例服用叶酸试验治疗,对比值有显著差异。检测组ＳＣＥ表达频率为３．６％,对照组子代ＳＣＥ表达频率为２．８％;服用叶酸检测ＳＣＥ表达频率为５．７％,未服用叶酸检测组ＳＣＥ表达频率为７．３％;研究数据提示被动吸烟有诱发ＳＣＥ表达频率增高,从而使染色体不稳定性增加,染色体畸变率增高。ＳＣＥ表达频率频繁的染色体及部位     

溴氰菊酯对白纹伊纹（Aedes albopictus）C6／36细胞株的…

本研究地选择１０μｇ／ｍｌ，２０μｇ／ｍｌ，４０μｇ／ｍｌ浓度的溴氰菊酯处理白纹伊蚊Ｃ６／３６细胞，以ＭＭＣ作为阳性对照物，观察溴氰菊酯处理２４ｈ后对Ｃ６／３６细胞当色体畸变率和姐妹染色单体互换（ＳＣＥ）频率的影响，结果显示，三个的浓度的溴氰菊酯对Ｃ６／３６细胞染色体畸变率均没有显著影响（Ｐ〈０．０５）；溴氰菊酯浓度在４０μｇ／ｍｌ时可诱导Ｃ６／３６细胞ＳＣＥ频率轻度增高（Ｐ〉０．０５），而溴氰菊     

异丙嗪对家兔EGTA性发热的解热作用及其机制研究

目的：观察异丙嗪（ｐｒｏｍｅｔｈａｚｉｎｅ,ＰＭＺ）对家兔ＥＧＴＡ性发热的影响并探讨其作用机制。方法：侧脑室和静脉给药。用Ｆｕｒａ－２荧光分光光度法测定细胞内游离钙浓度（［Ｃａ２＋］ｉ）。结果：（１）侧脑室灌注０６μｍｏｌＥＧＴＡ引起家兔明显的发热反应,侧脑室灌注０６μｍｏｌＥＧＴＡ２０ｍｉｎ后,静脉注射ＰＭＺ（５ｍｇ／ｋｇ）明显抑制ＥＧＴＡ引起的结肠温度上升,其３ｈ发热反应指数明显低于侧脑室灌注０６μｍｏｌＥＧＴＡ２０ｍｉｎ后静脉注射生理盐水（ＮＳ）组。而侧脑室灌注人工脑脊液（ＡＣＳＦ）２０ｍｉｎ后静脉注射ＰＭＺ（５ｍｇ／ｋｇ）组家兔结肠温度明显低于ＡＣＳＦ＋ＮＳ对照组。（２）体外实验发现,向下丘脑细胞悬液中加入终浓度为０７４ｍｍｏｌ／Ｌ的ＰＭＺ,下丘脑细胞［Ｃａ２＋］ｉ从（１５９２±１８８）ｎｍｏｌ／Ｌ升高到（５３３７±９０１）ｎｍｏｌ／Ｌ（Ｐ＜００５）。结论：ＰＭＺ诱导体温调节中枢神经细胞［Ｃａ２＋］ｉ升高可能是ＰＭＺ抑制家兔ＥＧＴＡ性发热的中枢机制之一。     

新疆塔什库尔干地区高原新生儿染色体畸变观察

目的：了解高原低氧分压对新生儿染色体畸变的影响。方法：收集新生儿脐带血（高原１６例,对照组５０例）常规培养、制片、Ｇ式显带、计数观察。结果：（１）高原组１６例新生儿中,染色体结构发生改变１０例,占６２５％,明显高于对照组１６０％（８／５０）（Ｐ＜０．０１）。（２）高原组新生儿染色体计数观察１５９４个,发生畸变８３个,占５２０７％;对照组共计数观察５００２个,发生畸变９４个,占１８７９％,两组比较有极高度显著性差异（Ｐ＜０．０１）。（３）高原组新生儿染色体结构异常占２１３３％（３４／１５９４）,其中内复制６个,双微体１４个,碎片断１０个,着丝粒爆开１个,断裂或增加３个,明显高于对照组０４２％（２１／５００２）（Ｐ＜０．０１）。（４）高原新生儿染色体数目异常占３０７％（４９／１５９４）,明显高于对照组１４５９％（７３／５００２）（Ｐ＜０．０１）。结论：高原新生儿染色体畸变率增加可能与高原低氧分压有关。     

皮下埋植Norplant Ⅰ 型避孕药囊妇女的细胞遗传学研究

对２９例皮下埋植ＮｏｒｐｌａｎｔⅠ型避孕药囊（芬兰产）已４年的妇女和１９例未埋药的正常妇女的外周血淋巴细胞培养后进行了细胞遗传学分析。研究结果分析表明：埋药组染色体畸变率明显高于对照组染色体畸变率，且有统计学意义（Ｐ＜０．０１）；埋药组ＳＣＥ频率平均值高于对照组ＳＣＥ频率平均值，且有统计学意义（Ｐ＜０．０５）；埋药组细胞微核率平均值虽高于对照组细胞微核率平均值，但无统计学意义（Ｐ＞０．０５）。研究结果提示：应引起对于长期皮下埋植ＮｏｒｐｌａｎｔⅠ型是否存在致突变作用问题的重视和研究。     

鼠抗粒细胞集落刺激因子单克隆抗体的研制

本文运用杂支瘤技术，成功地建立了６株能稳定分泌小鼠杭重组人粒细胞集落刺激因子（Ｇ－ＣＳＦ）单克隆抗体的杂交瘤细胞１Ｂ９Ｄ１０、１ＧＳＦ１０、２Ｃ８Ｃ１、２Ｅ４Ｆ６、３Ｃ６Ｅ１１、７Ｄ２Ｃ７）。试验结果表明，６株单抗均为１ｇＧ类，且特异性强，能分别识别不同的抗原结合位点，相对亲和力２Ｅ４Ｆ６单抗最高，１ＧＳＦ１０最低，为今后Ｇ－ＣＳＦ单抗的应用打下了基础。     

无症状心肌缺血和心绞痛患者血浆中内皮素、降钙素基因相关肽和P物质含量的变化

本文测定了无症状心肌缺血（ＳＭＩ）组（１４例）、心绞痛组（１１例）和对照组（７例）运动试验前后血浆内皮素（ＥＴ）、降钙素基因相关肽（ＣＧＲＰ）和Ｐ物质（ＳＰ）的含量，探讨了这３种肽类物质在ＳＭＩ和心绞痛发生中作用的差异。结果显示：运动前３组之间血浆ＥＴ含量比较无显著性差异，运动后３组组血浆ＥＴ含量分别为７７．７０±１８．４４，１１１．３３±２４．８２，９４．３８±１２．５９ｎｇ／Ｌ心绞痛组显著高于ＳＭＩ组（Ｐ＜０．０１）．运动前３组之间和运动后３组之间血浆ＣＧＲＰ含量比较均无显著性差异。运动前３组之间血浆ＳＰ含量比较无显著性差异，运动后３组血浆ＳＰ含量分别为２．２５±０．２１、２．４６±０．２０、２．１８±０．１２ｎｍｏｌ／Ｌ，心绞痛组明显高于ＳＭＩ组（Ｐ＜０．０５）和对照组（Ｐ＜０．０１）．结果提示：血浆ＥＴ、ＳＰ含量升高可能参与了心绞痛的发生，而心肌缺血时无症状可能与血浆ＥＴ、ＳＰ未升高有关。     

Opportunities and challenges in the prevention and control of cancer and other chronic diseases: children's diet and nutrition and weight and physical activity

OBJECTIVE: The purpose of this article is to review the role of behavioral research in disease prevention and control, with a particular emphasis on lifestyle- and behavior-related cancer and chronic disease risk factors--specifically, relationships among diet and nutrition and weight and physical activity with adult cancer, and tracking developmental origins of these health-promoting and health-compromising behaviors from childhood into adulthood. METHOD: After reviewing the background of the field of cancer prevention and control and establishing plausibility for the role of child health behavior in adult cancer risk, studies selected from the pediatric published literature are reviewed. Articles were retrieved, selected, and summarized to illustrate that results from separate but related fields of study are combinable to yield insights into the prevention and control of cancer and other chronic diseases in adulthood through the conduct of nonintervention and intervention research with children in clinical, public health, and other contexts. RESULTS: As illustrated by the evidence presented in this review, there are numerous reasons (biological, psychological, and social), opportunities (school and community, health care, and family settings), and approaches (nonintervention and intervention) to understand and impact behavior change in children's diet and nutrition and weight and physical activity. CONCLUSIONS: Further development and evaluation of behavioral science intervention protocols conducted with children are necessary to understand the efficacy of these approaches and their public health impact on proximal and distal cancer, cancer-related, and chronic disease outcomes before diffusion. It is clear that more attention should be paid to early life and early developmental phases in cancer prevention.     

Pain and Effusion and Quadriceps Activation and Strength

Context:

Quadriceps dysfunction is a common consequence of knee joint injury and disease, yet its causes remain elusive.

Objective:

To determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion affect the magnitude of quadriceps dysfunction.

Design:

Crossover study.

Setting:

University research laboratory.

Patients or Other Participants:

Fourteen (8 men, 6 women; age = 23.6 ± 4.8 years, height = 170.3 ± 9.16 cm, mass = 72.9 ± 11.84 kg) healthy volunteers.

Intervention(s):

All participants were tested under 4 randomized conditions: normal knee, effused knee, painful knee, and effused and painful knee.

Main Outcome Measure(s):

Quadriceps strength (Nm/kg) and activation (central activation ratio) were assessed after each condition was induced.

Results:

Quadriceps strength and activation were highest under the normal knee condition and differed from the 3 experimental knee conditions (P < .05). No differences were noted among the 3 experimental knee conditions for either variable (P > .05).

Conclusions:

Both pain and effusion led to quadriceps dysfunction, but the interaction of the 2 stimuli did not increase the magnitude of the strength or activation deficits. Therefore, pain and effusion can be considered equally potent in eliciting quadriceps inhibition. Given that pain and effusion accompany numerous knee conditions, the prevalence of quadriceps dysfunction is likely high.Key Words: arthrogenic muscle inhibition, central activation failure, voluntary activation, muscles

Key Points

• Knee pain and effusion resulted in arthrogenic muscle inhibition and weakness of the quadriceps.
• The simultaneous presence of pain and effusion did not increase the magnitude of quadriceps dysfunction.
• To reduce arthrogenic muscle inhibition and improve muscle strength, clinicians should employ interventions that target removing both pain and effusion.

Quadriceps weakness is a common consequence of traumatic knee joint injury^1,2 and chronic degenerative knee joint conditions.^3,4 Arthrogenic muscle inhibition (AMI), a neurologic decline in muscle activation, results in quadriceps weakness and hinders rehabilitation by preventing gains in strength.⁵ The inability to reverse AMI and restore muscle function can lead to decreased physical abilities,⁶ biomechanical deficits,⁷ and possibly reinjury.⁵ Furthermore, researchers^8,9 have suggested that quadriceps weakness resulting from AMI may place patients at risk for developing osteoarthritis in the knee. In light of the substantial influence of quadriceps AMI on these clinically relevant outcomes, we need to improve our understanding of the factors that contribute to this neurologic decline in muscle activity so efforts to target and reverse it can be implemented and gains in strength can be achieved more easily.Joint injury and disease are accompanied by numerous sequelae (ie, pain, swelling, tissue damage, inflammation), so ascertaining which one ultimately leads to neurologic muscle dysfunction is difficult. Whereas a joint effusion can result in AMI,^10–12 the effects of pain are less understood despite many clinicians attributing AMI to pain. Using techniques that introduce knee pain without accompanying injury may provide insights into the role of pain in eliciting AMI.The degree of knee joint damage may play a role in the quantity of AMI that manifests. Hurley et al^13,14 demonstrated that quadriceps AMI, measured using an interpolated-twitch technique, was greater in patients with extensive traumatic knee injury (eg, fractured tibial plateau, ruptured medial collateral ligament, and medial meniscectomy) than patients with isolated joint trauma (ie, isolated anterior cruciate ligament [ACL] rupture). Similarly, patients with more knee joint symptoms (ie, greater number of symptoms and increased severity of symptoms) may present with greater magnitudes of quadriceps inhibition. Recently, investigators¹⁵ have suggested that patients with more pain display less quadriceps strength, supporting this tenet. Given that effusion and pain often present simultaneously with joint injuries and diseases, such as ACL injury and osteoarthritis, examining both the isolated and cumulative effects of these sequelae appears warranted to determine if they influence the magnitude of muscle inhibition.Experimental joint-effusion and pain models are safe and effective experimental methods that allow for the isolated examination of their effects on muscle function. The effusion model, whereby sterile saline is injected directly into the knee joint capsule,⁷ produces a clinically relevant magnitude of the joint effusion that may be present with traumatic injury. Effusion is thought to activate group II afferents responding to stretch or pressure,^16–18 which in turn may facilitate group Ib interneurons and result in quadriceps AMI.⁵ The pain model involves injecting hypertonic saline into the infrapatellar fat pad to produce anteromedial knee pain similar to that described in patients with patellofemoral pain syndrome.¹⁹ Pain is considered to initiate AMI through activation of group III and IV afferents that act as nocioceptors to signal damage or potential damage to joint structures.^16–18 The firing of these afferents then may lead to facilitation of group Ib interneurons, the flexion reflex, or the gamma loop, ultimately resulting in quadriceps inhibition.²⁰ Thus, these models allow us to create symptoms that are associated with knee injury and have the added benefit of providing a way to examine their effects in isolation.Therefore, the purpose of our study was to determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion would affect the magnitude of quadriceps dysfunction. We hypothesized that pain alone would result in quadriceps inhibition and that the magnitude of inhibition would be greater when effusion and pain were present simultaneously.     

Postinfectious immunodeficiency and autoimmunity: pathogenic and clinical values and implications

Autoimmunity is still a mystery of clinical immunology and medicine as a whole. The etiology and pathogenesis of autoimmune disorders remain unclear and, thus, are assessed as a balance between hereditary predisposition, triggering factors and the appearance of autoantibodies and/or self-reactive T cells. Among the immunological armamentarium, molecular mimicry, based on self-reactive T- and B-cell activation by cross-reactive epitopes of infectious agents, is of special value. Hypotheses regarding the possible involvement of molecular mimicry in the development of postinfectious autoimmunity are currently very intriguing. They provide new approaches for identifying etiological agents that are associated with postinfectious autoimmunity, paired microbial- and tissue-linked epitopes targeted for autoimmune reaction determination, postinfectious autoimmunity pathogenesis recognition and specific prevention, and therapy for autoimmune disorder development.     

Beta-endorphin and drug-induced reward and reinforcement

Although drugs of abuse have different acute mechanisms of action, their brain pathways of reward exhibit common functional effects upon both acute and chronic administration. Long known for its analgesic effect, the opioid beta-endorphin is now shown to induce euphoria, and to have rewarding and reinforcing properties. In this review, we will summarize the present neurobiological and behavioral evidences that support involvement of beta-endorphin in drug-induced reward and reinforcement. Currently, evidence supports a prominent role for beta-endorphin in the reward pathways of cocaine and alcohol. The existing information indicating the importance of beta-endorphin neurotransmission in mediating the reward pathways of nicotine and THC, is thus far circumstantial. The studies described herein employed diverse techniques, such as biochemical measurements of beta-endorphin in various brain sites and plasma, and behavioral measurements, conducted following elimination (via administration of anti-beta-endorphin antibodies or using mutant mice) or augmentation (by intracerebral administration) of beta-endorphin. We suggest that the reward pathways for different addictive drugs converge to a common pathway in which beta-endorphin is a modulating element. beta-Endorphin is involved also with distress. However, reviewing the data collected so far implies a discrete role, beyond that of a stress response, for beta-endorphin in mediating the substance of abuse reward pathway. This may occur via interacting with the mesolimbic dopaminergic system and also by its interesting effects on learning and memory. The functional meaning of beta-endorphin in the process of drug-seeking behavior is discussed.     

PTEN与信号转导及肿瘤

ＴＥＮ[1] (ｐｈｏｓｐｈａｔａｓｅａｎｄｔｅｎｓｉｎｈｏｍｏｌｏｇｙｄｅｌｅｔｅｄｏｎｃｈｒｏｍｏｓｏｍｅｔｅｎ)又名ＭＭＡＣ1 [2 ] (ｍｕｔａｔｅｄｉｎｍｕｔｉｐｌｙａｄａｎｃｅｄｃａｎｃｅｒ 1 )和ＴＥＰ1 [3 ] (ＴＧＦ -βｒｅｇｕｌａｔｅｄａｎｄｅｐｉｔｈｅｌｉａｌｃｅｌｌ -ｒｉｃｈｅｄｐｈｏｓｐｈａｔａｓｅ 1 ) (以下均称为ＰＴＥＮ) ,是 1 997年由 3个研究小组先后发现的一个具有双特异磷酸酶活性的抑癌基因。ＰＴＥＮ基因异常广泛存在于人类多种恶性肿瘤 ,如恶性神经胶质瘤、前列腺癌、子宫内膜癌、黑色素瘤等…     

Tobacco and alcohol and the risk of head and neck cancer

Summary We carried out two case-control studies on the relative risk of head and neck cancer in association with tobacco and alcohol consumption. The first study carried out at the ENT Department of the University hospitals of Heidelberg and Giessen (FRG) comprised 200 male patients with squamous cell cancer of the head and neck and 800 control subjects matched for sex, age, and residential area (1:4 matching design). Of the tumour patients, 4.5% had never smoked, in contrast to 29.5% of the control group. The average tobacco and alcohol consumption of the patients was approximately twice as high as in the control subjects. The highest alcohol and tobacco consumption was observed in patients suffering from oropharyngeal cancer. Tobacco and alcohol increased the risk of head and neck cancer in a dose-dependent fashion and acted as independent risk factors. In heavy smokers (> 60 pack-years) a relative risk of 23.4 (alcohol adjusted) was calculated. Combined alcohol and tobacco consumption showed a synergistic effect. The risk ratio increased more in a multiplicative than in an additive manner. Oral and laryngeal cancer were associated with the highest tobacco-associated risk values. The highest ethanol-associated risk values were associated with oropharyngeal and laryngeal cancer. The second study was carried out at the ENT Department of the University of Heidelberg on 164 males with squamous cell carcinoma of the larynx and 656 control subjects matched for sex, age and residential area (1:4 matching design). Of the cases, 4.2% had never smoked, compared with 28.5% of the control subjects. The risk of laryngeal cancer by tobacco consumption was dose dependent, reaching a maximum value of 9.1 (adjusted for alcohol) for a consumption of more than 50 tobacco-years (TY). The relative risk of laryngeal cancer associated with alcohol intake was also dose dependent, reaching a value of 9.0 (adjusted for tobacco) for a mean daily consumption of more than 75 g alcohol. An analysis of subsite specific risks showed that heavy smokers (> 50 TY) carried a nearly ten times higher risk of supraglottic cancer than of glottic cancer. The risk of supraglottic cancer from alcohol consumption was also higher than that of glottic cancer.     

Muscle strength and serum testosterone,cortisol and SHBG concentrations in middle-aged and elderly men and women

Forty healthy males (M) and females (F) divided into two different age groups i.e. M50 years (range 44–57; n= 9), F50 years (range 43–54; n= 9), M70 years (range 64–73; n= 11) and F70 years (range 63–73; n= 11) volunteered as subjects for examination of muscle cross-sectional area (CSA) and maximal voluntary isometric force production characteristics of the leg extensor muscles and serum androgen and sex hormone binding globulin (SHBG) concentrations. The CSA in the male groups was greatly larger (P < 0.01) than in the female groups and both elderly groups demonstrated slightly (n.s.) smaller values in the CSA than the two middle-aged groups. Maximal force of 2854 ± 452 N in M50 was greater (P < 0.05) than that of 2627 ± 752 N recorded for F50 as well as the force of 2787 ± 843 in M70 was greater (P < 0.001) than that of 1849 ± 295 recorded for F70. The force between F50 and F70 differed significantly (P < 0.05) from each other. The maximal rate of force production in M50 was greater (P < 0.01) than in F50 as well as in M70 greater (P < 0.001) than in F70. Both middle-aged groups demonstrated greater (P < 0.05) values than the respective elderly groups of the same sex. The individual values in the CSA correlated with the values in maximal force both in the middle-aged subjects (r= 0.66; P < 0.01) and in the elderly subjects (r= 0.69; P < 0.01). The mean concentration of serum testosterone in M50 was slightly (n.s.) greater than in M70 and in F50 significantly (P < 0.05) greater than in F70. Serum SHBG levels were lower in the males (P < 0.01) than in the females and serum testosterone/SHBG ratio in M70 and in F70 were lower (P < 0.05) than in M50 and in F50, respectively. In the females significant positive correlations were observed between the individual values in serum testosterone concentration and the values both in the CSA (r= 0.46; P < 0.05) and in maximal force (r= 0.62; P < 0.01) as well as between serum testosterone/SHBG ratio and both the CSA (r= 0.55; P < 0.05) and maximal force (r= 0.68; P < 0.01). The present results imply that the decreasing basal level of blood testosterone over the years in aging people, especially in females, may lead to decreasing anabolic effects on muscles thus having an association with age-related declines in the maximal voluntary neuromuscular performance capacity in aging people.     

Platelet-activating factor receptor and respiratory and metabolic responses to hypoxia and hypercapnia

Activation of the platelet-activating factor receptor (PAFR) regulates neural transmission. A PAFR blocker reduced the peak hypoxic (pHVR) but not hypercapnic ventilatory (HCVR) responses in rats [Am. J. Physiol. 275 (1998) R604]. To further examine the role of PAFR in respiratory control, genotype-verified PAFR -/- and PAFR +/+ adult male mice underwent hypoxic and hypercapnic challenges. HCVR was similar in the two groups (p-NS). However, pHVR was significantly reduced in PAFR -/- mice (38 +/- 13% baseline [S.D.]) compared to PAFR +/+ mice (78 +/- 16% baseline; P < 0.001, ANOVA), with reduced tidal volume recruitments during pHVR. In addition, hypoxic ventilatory depression was attenuated in PAFR -/- mice (P < 0.01), and was primarily due to attenuation of the time-dependent decreases in oxygen consumption during sustained hypoxia (P < 0.01). Thus, PAFR expression/function modulates components of the acute ventilatory and metabolic adaptations to hypoxia but not to hypercapnia. Imbalances in PAFR activity may lead to maladaptive regulation of the tightly controlled metabolic-ventilatory relationships during hypoxia.