阻塞性睡眠呼吸暂停低通气综合征患者动脉粥样硬化无创检测指标分析

目的检测血流介导的血管扩张(FMD)、脉搏波传导速度(PWV)和颈动脉内膜中层厚度(CIMT),探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)与动脉粥样硬化之间的关系。方法对76例OSAHS患者(OSAHS组)及76例年龄、性别、体重指数与之相匹配患者(对照组)进行FMD、PWV和CIMT检测,对两组间FMD、PWV和CIMT值进行比较,对OSAHS组睡眠呼吸暂停低通气指数(AHI)与FMD、PWV和CIMT之间关系进行相关性分析。结果OSAHS组PWV[(1720±247)cm/s]、CIMT[(1.10±0.34)mm]显著高于对照组[(1469±172)cm/s、(0.80±0.18)mm],FMD[(5.8±1.7)%]显著低于对照组[(8.9±1.4)%,P均<0.01];比较两组中所有伴高血压者,OSAHS组PWV、CIMT[(1850±244)cm/s、(1.24±0.35)mm]仍显著高于对照组[(1655±161)cm/s、(0.99±0.18)mm,P=0.001、0.003],FMD[(5.2±1.7)%]显著低于对照组[(7.5±1.1)%,P<0.01];OSAHS组AHI值与PWV、CIMT值呈正相关(r=0.883、0.698,P均<0.01),与FMD值呈负相关(r=-0.711,P<0.01)。结论OSAHS患者存在更为明显的内皮功能障碍及动脉粥样硬化,且与OSAHS严重程度有关。     

血小板活化对老年阻塞性睡眠呼吸暂停低通气综合征患者的影响

目的探讨血小板活化在老年人阻塞性睡眠呼吸暂停低通气综合征(OSAHS)发生发展中的作用及经鼻持续气道正压通气(nCPAP)对其影响.方法选择经多导睡眠图(PSG)确诊的老年OSAHS患者90例为试验组,据睡眠呼吸暂停低通气指数(AHI)、最低血氧饱和度(SaO2)将OSAHS患者分轻、中、重3组,其中16例重度OSAHS患者接受nCPAP治疗为治疗组,并设健康对照组20例,用酶联免疫双抗体夹心法检测各组血浆α-颗粒膜蛋白(GMP-140)、血小板膜糖蛋白Ⅱb/Ⅲa(GPⅡb/Ⅲa),比较各试验组与对照组,治疗组治疗前、后的各项指标的差异.结果 (1)中、重度老年OSAHS患者组血浆GMP-140[(16.6±2.3)μg/L、(18.9±3.1)μg/L]、GPⅡb/Ⅲa(38 468±952/49673±1037、39 867±1264/50 899±2476)均显著高于对照组[(14.8±2.1)μg/L、37672±769/48469±1672, P ＜0.05],nCPAP治疗后比治疗前明显下降(P ＜0.001);(2)GMP-140、GPⅡb/Ⅲa与AHI呈正相关(r值为0.5273、0.4829/0.4562,均为P ＜0.001),与SaO2min呈负相关(r值为-0.6481、-0.5846/-0.6264,均为P ＜0.001).结论中、重度老年OSAHS患者存在明显血小板活化,并与夜间低氧血症密切相关,其可能在OSAHS患者心脑血管栓塞性并发症高发生率中起重要作用;nCPAP治疗可有效逆转上述改变.     

阻塞性睡眠呼吸暂停低通气综合征患者血清维生素D水平变化及其与疾病严重程度的相关性研究

目的分析阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血清维生素D水平变化及其与疾病严重程度的相关性。方法选取2015年4月—2017年5月本溪市中心医院收治的OSAHS患者40例作为观察组,根据呼吸暂停低通气指数(AHI)分为轻度(5次/h≤AHI20次/h)13例、中度(20次/h≤AHI40次/h)12例、重度(≥40次/h)15例;另选取同期于本溪市中心医院体检的健康肥胖者[体质指数(BMI)≥25.0 kg/m~2]40例作为对照组。比较两组受试者动脉血氧饱和度(SaO_2)、血清25-羟维生素D[25-(OH)D]水平及维生素D缺乏程度,不同严重程度OSAHS患者SaO_2及血清25-(OH)D水平;血清25-(OH)D水平与OSAHS患者AHI、SaO_2的相关性分析采用Pearson相关分析。结果 (1)观察组患者SaO_2及血清25-(OH)D水平低于对照组,维生素D缺乏程度劣于对照组(P0.05)。(2)中度和重度OSAHS患者SaO_2及血清25-(OH)D水平低于轻度OSAHS患者,重度OSAHS患者SaO_2及血清25-(OH)D水平低于中度OSAHS患者(P0.05)。(3)Pearson相关分析结果显示,血清25-(OH)D水平与OSAHS患者AHI呈负相关(r=-0.527,P=0.004),与SaO_2呈正相关(r=0.352,P=0.025)。结论OSAHS患者血清维生素D水平降低,维生素D不足或缺乏发生率较高,且维生素D水平与OSAHS严重程度呈负相关,维生素D可能参与OSAHS的发生发展。     

阻塞性睡眠呼吸暂停低通气综合征对患者心肌缺血负荷的影响

目的探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)对患者心肌缺血的影响及可能机制。方法纳入52例OSAHS患者和21名健康体检者,应用多导睡眠监测系统(PSG)行至少7 h睡眠呼吸监测,长程动态心电图(Holter)同步记录心电动态变化,分析心肌缺血与呼吸紊乱指数(AHI)的关系。结果轻中度OSAHS组(5次/h≤AHI<30次/h)与重度OSAHS组(AHI≥30次/h)均表现为睡眠时心肌缺血负荷显著大于觉醒时,且OSAHS患者AHI与睡眠时心肌缺血负荷相关(r=0.667,P<0.01)。轻中度OSAHS组与重度OSAHS组分别根据有无心肌缺血情况,分为心肌缺血组和无心肌缺血组。轻中度组亚组分析显示,与无心肌缺血组相比,心肌缺血组清醒时与睡眠时的平均心率均显著增快[(83.33±6.86)次/min比(76.30±8.52)次/min;(64.71±6.94)次/min比(59.18±2.94)次/min,均为P<0.05]。重度组亚组分析显示,与无心肌缺血组相比,心肌缺血组睡眠效率(74.71%±8.32%比86.36%±6.33%,P<0.01)、最低血氧饱和度(52.36%±17.32%比64.80%±14.86%,P<0.05)、平均血氧饱和度(87.93%±4.80%比92.00%±1.73%,P<0.01)及总非快速动眼期时间/总睡眠时间(68.67%±4.19%比76.87%±7.16%,P<0.05)均显著降低,SaO_2<90%的时间及最长呼吸暂停时间[(236.65±132.72)min比(124.10±82.99)min;(71.63±15.94)s比(55.28±22.05)s,均为P<0.05]均显著延长。结论 OSAHS患者睡眠时的心肌缺血与阻塞性睡眠呼吸暂停相关。轻中度OSAHS患者睡眠时心肌缺血可能由反复交感神经系统激活相关的改变所致,重度OSAHS患者的心肌缺血可能与低氧血症及睡眠结构紊乱相关。     

阻塞性睡眠呼吸暂停低通气综合征患者血尿酸变化的临床意义

目的:了解不同程度阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血尿酸水平的变化,并分析二者之间的相关性。方法:选择我院2007年3月至2009年7月就诊的OSAHS患者80例,根据睡眠监测得出的睡眠呼吸暂停低通气指数(AHI)分为轻度OSAHS组(5次/h≤AHI≤20次/h,27例)、中度OSAHS组(20次/h40次/h,34例)和对照组(AHI<5次/h,20例);观察各组年龄、性别、体质量指数(BMI)、血清胆固醇、甘油三脂、血糖、尿酸及睡眠各项指标变化,比较3组间各观察指标的差异;对OSAHS组血清尿酸水平与AHI、最低脉搏容积血氧饱和度(LSpO2)和氧减<90%的时间T90进行相关性分析。结果:组间年龄及性别相比差异均无统计学意义(P均>0.05)。轻、中度OSAHS组血尿酸水平分别为(365.30±92.37)μmol/L,(374.63±78.17)μmol/L均高于对照组(336.82±74.08)μmol/L,但差异无统计学意义;重度OSAHS组血清尿酸水平(440.26±92.14)μmol/L与对照组比较差异有统计学意义(P<0.01);OSAHS组血清尿酸水平与AHI、T90呈显著正相关(r值分别为0.441、0.309,P均<0.001)与LSpO2呈负相关(r值为-0.370,P<0.001)。结论:OSAHS患者中血清尿酸水平随着AHI的增加和缺氧程度的加重而增高,并与AHI、T90及LSpO2有较强的相关性。提示OSAHS患者反复发作低氧血症可能是心血管病高发的另一个原因。     

阻塞性睡眠呼吸暂停低通气综合征患者血浆食欲素A水平的变化及意义

目的探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆食欲素A的变化及意义。方法选择OSAHS并肥胖患者30例(OSAHS组)、单纯肥胖者30例(单纯肥胖组)和健康成人20名(正常对照组)。其中OSAHS组和单纯肥胖组的体重指数(BMI)均≥25kg/m2且差异无统计学意义。所有受试者均接受多导睡眠仪监测,采用层析及放射免疫法测定血浆食欲素A的水平。结果OSAHS组血浆食欲素A水平[(9.0±1.8)ng/L]显著高于单纯肥胖组[(7.2±1.4)ng/L,P<0.01]及正常对照组[(6.7±1.6)ng/L,P<0.01]。OSAHS组血浆食欲素A水平与呼吸暂停低通气指数(AHI)、微觉醒指数(arousalindex)呈正相关(r=0.639、0.435,P均<0.05),与最低血氧饱和度(LSaO2)、平均血氧饱和度(MSaO2)呈负相关(r=-0.521、-0.589,P均<0.01)。OSAHS组及单纯肥胖组血浆食欲素A水平与BMI无相关性(r=0.132,P>0.05)。结论OSAHS患者血浆食欲素A水平升高,其原因可能与患者夜间反复发作性低氧有关,且食欲素A在调节睡眠觉醒的过程中可能发挥了重要的作用。     

阻塞性睡眠呼吸暂停低通气患者血清纤溶酶原激活物抑制剂1水平与颈动脉内膜中膜厚度及斑块稳定性的关系

[目的]探索阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血清纤溶酶原激活物抑制剂1(PAI-1)水平与颈动脉内膜中膜厚度(CIMT)及斑块稳定性的相关性。[方法]收集宝鸡市中心医院2019年7月—2021年1月行多导睡眠监测(PSG)的167例患者,基于睡眠呼吸暂停低通气指数(AHI)分为对照组(46例)、轻度OSAHS组(15例)、中度OSAHS组(39例)和重度OSAHS组(67例),比较各组一般临床资料、PSG相关指标、血生物化学指标、血清PAI-1水平和CIMT的差异。分析OSAHS患者血清PAI-1水平与CIMT和动脉硬化斑块稳定性的关系,根据CIMT及颈动脉斑块形态和超声学特征将OSAHS患者分为单纯OSAHS组(37例)、OSAHS稳定性斑块组(46例)和OSAHS不稳定性斑块组(38例),比较各组患者PAI-1水平,多因素Logistic回归分析探索OSAHS患者颈动脉斑块稳定性的危险因素。[结果]对照组、轻度OSAHS组、中度OSAHS组和重度OSAHS组之间性别、体质指数(BMI)、高血压病、吸烟史、AHI、氧减指数(ODI)、氧饱和度低于90%的时间占睡眠期的...     

OSAHS对非老年2型糖尿病患者25羟维生素D3的影响

目的 探讨非老年2型糖尿病患者中OSAHS与25羟维生素D3 [25 (OH)D3]水平的关系.方法 根据睡眠呼吸暂停指数 (AHI),将158例2型糖尿病患者分为单纯糖尿病组 (T2DM组38例)、OSAHS轻度组 (OM-A组38例)、中度组 (OM-B组46例)及重度组 (OM-C组36例),比较各组间临床资料及25 (OH)D3等指标的差异及相关性.结果 T2DM组的 HOMA-IR显著低于OM-B组和 OM-C组,差异有统计学意义 (F=18.24,P <0.05).OM-C 组与 T2DM组在 TG的差异有统计学意义 (F=40.18,P<0.05).4组间在2hPG、25 (OH)D3及 SaO2min的差异有统计学意义 (F=29.54、32.16、24.27,P<0.05).相关分析提示25 (OH)D3水平与 AHI、2hPG 呈负相关 (P<0.05),与 SaO2min呈正相关 (P <0.05).结论 2型糖尿病患者25 (OH)D3水平与OSAHS有显著相关性.     

冠心病合并阻塞性睡眠呼吸暂停低通气综合征患者冠状动脉狭窄程度及血清胱抑素C的变化

目的观察冠心病合并阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者的冠状动脉狭窄程度及血清胱抑素C(CysC)的变化。方法采用回顾性研究的方法,纳入162例冠心病且有夜间睡眠打鼾、呼吸暂停或白天嗜睡症状的患者,根据睡眠监测结果分为单纯冠心病组(C组)62例[呼吸暂停低通气指数(AHI)<5次/h]和冠心病合并OSAHS组(CO组)100例(AHI≥5次/h),再依据AHI将CO组分为轻度组24例、中度组28例和重度组48例;另以冠状动脉造影证实狭窄<50%且否认夜间睡眠打鼾的患者52例为对照组(N组)。计算Gensini评分评估冠状动脉狭窄程度,检测空腹血清CysC水平。采用SPSS 20.0统计软件比较各组间冠状动脉狭窄程度及血清CysC水平的差异。结果 CO组Gensini评分高于N组和C组(23.58±25.78比2.47±2.91和13.89±24.19,P<0.01和P<0.05),且重度OSAHS组Gensini评分高于轻度组(27.71±28.26比15.71±18.22,P<0.05);CO组血清CysC水平高于N组和C组[(1.02±0.20)mg/L比(0.87±0.14)mg/L和(0.87±0.18)mg/L,均为P<0.05],且重度OSAHS组血清CysC水平高于轻度组和中度组[(1.10±0.17)mg/L比(0.89±0.15)mg/L和(1.02±0.21)mg/L,P<0.01和P<0.05]。结论冠心病合并OSAHS患者的血清CysC水平高于单纯冠心病患者和无冠心病者;冠心病合并OSAHS患者的冠状动脉狭窄程度较单纯冠心病患者严重。     

阻塞性睡眠呼吸暂停低通气综合征患者骨代谢标志物、甲状腺功能的变化及相关性

目的通过测定阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者及非OSAHS患者血清一般生化标志物:钙、镁、磷;骨代谢调控激素:血清25羟-维生素D〔(25(OH)D〕、甲状旁腺激素(PTH);骨转换标志物:总Ⅰ型胶原氨基端延长肽(tPINP)、β-胶原特殊序列(CTX)及血清游离三碘甲状原氨酸(FT3)、血清游离甲状腺素(FT4)、血清促甲状腺激素(TSH),明确不同程度OSAHS患者骨代谢标志物的变化规律及与甲状腺相关激素是否存在相关性。方法行多导睡眠监测(PSG)确诊为OSAHS的患者89例,根据呼吸暂停低通气指数(AHI)分为轻、中、重度组3组,轻度组29例、中度组30例,重度组30例,对照组为排除OSAHS患者36例,记录所有受试者一般资料及骨代谢标志物指标及FT3、FT4、TSH,比较各组的差异及与AHI的相关性分析。结果中、重度组患者β-CTX、tPINP值较对照组及轻度组显著升高,差异有统计学意义(P<0.05),Pearson相关分析显示OSAHS组患者体重指数(BMI)、β-CTX、tPINP水平与AHI呈显著正相关(P<0.05),FT3、FT4、TSH与AHI无相关性(P>0.05)。结论缺氧参与骨质疏松发病过程,OSAHS患者存在骨代谢异常。     

Three layer functional model and energy exchange concept of aging process

Relying on a certain degree of abstraction, we can propose that no particular distinction exists between animate or living matter and inanimate matter. While focusing attention on some specifics, the dividing line between the two can be drawn. The most apparent distinction is in the level of structural and functional organization with the dissimilar streams of ‘energy flow’ between the observed entity and the surrounding environment. In essence, living matter is created from inanimate matter which is organized to contain internal intense energy processes and maintain lower intensity energy exchange processes with the environment. Taking internal and external energy processes into account, we contend in this paper that living matter can be referred to as matter of dissipative structure, with this structure assumed to be a common quality of all living creatures and living matter in general. Interruption of internal energy conversion processes and terminating the controlled energy exchange with the environment leads to degeneration of dissipative structure and reduction of the same to inanimate matter, (gas, liquid and/or solid inanimate substances), and ultimately what can be called ‘death.’ This concept of what we call dissipative nature can be extended from living organisms to social groups of animals, to mankind. An analogy based on the organization of matter provides a basis for a functional model of living entities. The models relies on the parallels among the three central structures of any cell (nucleus, cytoplasm and outer membrane) and the human body (central organs, body fluids along with the connective tissues, and external skin integument). This three-part structural organization may be observed almost universally in nature. It can be observed from the atomic structure to the planetary and intergalactic organizations. This similarity is corroborated by the membrane theory applied to living organisms. According to the energy nature of living matter and the proposed functional model, the decreased integrity of a human body's external envelope membrane is a first cause of the structural degradation and aging of the entire organism. The aging process than progresses externally to internally, as in single cell organisms, suggesting that much of the efforts towards the restoration and maintenance of the mechanisms responsible for structural development should be focused accordingly, on the membrane, i.e., the skin. Numerous reports indicate that all parts of the human body, like: bones, blood with blood vessels, muscles, skin, and so on, have some ability for restoration. Therefore, actual revival of not only aging tissue of the human body's membrane, but the entire human body enclosed within, with all internal organs, might be expected. We assess several aging theories within the context of our model and provide suggestions on how to activate the body's own anti-aging mechanisms and increase longevity. This paper presents some analogies and some distinctions that exist between the living dissipative structure matter and inanimate matter, discusses the aging process and proposes certain aging reversal solutions.     

Unusual responses of nocturnal pineal melatonin synthesis and secretion to swimming: Attempts to define mechanisms

Abstract: The effect of swimming at night on rat pineal melatonin synthesis was compared with that of light exposure at night. Rats were forced to swim at 0030 hr (lights out at 2000 hr) and sacrificed by decapitation 15 and 30 min later, immediately after swimming. Other groups of animals were exposed to white light (650μW/cm²) for 15 and 30 min at same time. Swimming caused a rapid and highly significant drop in the melatonin content in the pineal gland; however, the activity of N-acetyltransferase (NAT), the supposed rate limiting enzyme in the melatonin production, was not changed. Despite the drop in pineal melatonin levels, serum concentrations of the indole remained elevated in the rats that swam. In contrast, melatonin levels in the pineal and serum of light exposed rats fell precipitously, accompanied by a significant suppression of NAT activity. Since we anticipated that the strenuous exercise associated with swimming may induce release of artrial natriuretic peptide (ANP) from the heart, which in turn could cause the release of pineal melatonin, in a second study we injected physiological saline intravenously to stretch the cardiac muscle and release ANP. Three milliliters of normal saline was injected during the day into the jugular vein of anesthetized rats that were pretreated with isoproterenol to stimulate pineal melatonin production. Animals were killed 15 min after the saline injection, and pineal NAT activity and pineal melatonin levels were measured. The saline injections caused no alteration in the elevated levels of either NAT or melatonin. These data suggest that the disparity in pineal NAT activity (which was high) and pineal melatonin (which was low), in animals swum at night, may not be caused by ANP which is released during strenuous exercise such as swimming.     

The immunoneuroendocrine role of melatonin

Abstract: A tight, physiological link between the pineal gland and the immune system is emerging from a series of experimental studies. This link might reflect the evolutionary connection between self-recognition and reproduction. Pinealectomy or other experimental methods which inhibit melatonin synthesis and secretion induce a state of immunodepression which is counteracted by melatonin. In general, melatonin seems to have an immunoenhancing effect that is particularly apparent in immunodepressive states. The negative effect of acute stress or immunosuppressive pharmacological treatments on various immune parameters are counteracted by melatonin. It seems important to note that one of the main targets of melatonin is the thymus, i.e., the central organ of the immune system. The clinical use of melatonin as an immunotherapeutic agent seems promising in primary and secondary immunodeficiencies as well as in cancer immunotherapy. The immunoenhancing action of melatonin seems to be mediated by T-helper cell-derived opioid peptides as well as by lymphokines and, perhaps, by pituitary hormones. Melatonin-induced-immuno-opioids (MHO) and lymphokines imply the presence of specific binding sites or melatonin receptors on cells of the immune system. On the other hand, lymphokines such as -γ-interferon and interleukin-2 as well as thymic hormones can modulate the synthesis of melatonin in the pineal gland. The pineal gland might thus be viewed as the crux of a sophisticated immunoneuroendocrine network which functions as an unconscious, diffuse sensory organ.     

Melatonin and photoperiodic time measurement: Seasonal breeding in the sheep

Abstract: Well-established circadian physiology supports the view that photoperiodic time measurement utilizes the coincidence between the presence of light and a photosensitive phase of a 'biological clock' to alter reproductive status—the so-called external coincidence model of seasonal breeding. In this review, we examine the mechanism whereby photoperiod interacts with presumed suprachiasmatic nuclei activity to allow endogenous melatonin to normally synchronize reproductive activity to the optimal time of year. The Romney Marsh sheep is particularly explored as an experimental model. It is suggested that the on/off activity of seasonal reproduction may be a robust mechanism able to be predictably manipulated by the judicious use of the light/dark cycle and exogenous melatonin, but firmly based on circadian principles.     

Response of rat pineal melatonin to calcium, magnesium, and lithium is circadian stage dependent

Abstract: Herein we documented the response of pineal melatonin production to electrolytes known to be effective on pineal function in view of a possible circadian stage dependence. We studied the release of melatonin by perifused rat pineal glands at 2 different circadian stages corresponding to the middle of the light and dark periods, i.e., respectively, 7 and 19 HALO (Hours After Light Onset, L:D = 12:12). The initial efflux rates were, as expected, much higher in the perifusates of glands removed from rats sacrificed during the dark phase than of those removed during the light phase. After 3 hr of perifusion, melatonin release reached similar levels which were found constant up to the 8th hr of perifusion, whatever the circadian stage. Perifusion of the glands with physiological concentrations for the rat of calcium (5.2 mmol/1) and magnesium (1.34 mmol/1) resulted in a stimulatory effect on the pineal glands removed from rats sacrificed in the middle of the dark period (19 HALO), whereas no effects were observed on the pineal glands removed from rats sacrificed during the light (7 HALO). Lithium (0.28 and 0.55 mmol/1) was ineffective on melatonin release in pineal glands removed 7 and 19 HALO. Our results show differences in the initial efflux rates of melatonin and in the response of perifused pineal glands to calcium and magnesium according to the circadian stage.     

Conservative management of perforated duodenal diverticulum： A case report and review of the literature

Duodenal diverticula are a relatively common condition. They are asymptomatic, unless they become complicated, with perforation being the rarest but most severe complication. Surgical treatment is the most frequently performed approach. We report the case of a patient with a perforated duodenal diverticulum, which was diagnosed early and treated conservatively with antibiotics and percutaneous drainage of secondary retroperitoneal abscesses. We suggest this method could be an acceptable option for the management of similar cases, provided that the patient is in good general condition and without septic signs.     

Changes in connexin43, the gap junction protein of astrocytes, during development of the rat pineal gland

Abstract: The abundance of gap junctions between rat pineal astrocytes formed by connexin43 (Cx43) was studied during development. Levels and distribution of Cx43 were measured by immunoblotting and indirect immunofluorescence, respectively. The amount of Cx43 in cells located within the gland was low until about the 7th postnatal day and increased to adult values between the 14th and 21st days postpartum. Although astrocytes, recognized by their vimentin immunoreactivity, were scarce before birth, they were abundant by the 7th postnatal day suggesting that the low levels of Cx43 found at this age corresponded to a low expression of this protein. Localization of the immunoreactivity to Cx43 and vimentin showed a close correlation, indicating that mature or immature pineal astrocytes form gap junctions made of Cx43. Since Cx43 levels attained their adult values at about the time the innervation and the functional state of the gland reached maturity (2–3 weeks after birth), it is proposed that astrocyte gap junctions are involved in the function of the adult rat pineal gland.