缺氧缺血对新生大鼠及小鼠脑细胞线粒体膜电势的影响

目的了解缺氧缺血(HI)对新生大鼠及新生小鼠脑细胞线粒体膜电势(ΔΨm)的影响。方法7日龄SD大鼠和C57小鼠各160只,分为正常对照组和HIBD后0、1、3、4、8、12h和24h组(各组n=20,其中10只测定海马、大脑皮质、丘脑部位的ΔΨm值),HIBD动物予以右颈总动脉分离结扎再置8%O2低氧舱处理,以流式细胞仪测定ΔΨm,比较同一动物HI损伤侧(右侧,即A侧)与损伤对侧(B侧)之间ΔΨm的比值(即A、BΔΨm比值)变化。结果HI损伤后新生SD大鼠及C57小鼠脑细胞ΔΨm均呈现“降低恢复再降低再恢复再降低”的改变,新生SD大鼠A、B侧ΔΨm比值在HI后0、4、24h出现3次降低,分别为(0.80±0.17)、(0.70±0.22)、(0.71±0.13),新生C57小鼠的该比值在HI后0、24h出现2次降低,分别为(0.84±0.26)、(0.86±0.13);新生SD大鼠改变最明显的部位是大脑皮质区,其HI后0、4、24h的比值为(0.69±0.07)、(0.73±0.11)、(0.65±0.20),新生C57小鼠改变最明显的部位是海马回,其HI后0、4、24h的比值为(0.71±0.16)、(0.71±0.21)、(0.76±0.20);新生SD大鼠和C57小鼠丘脑区的ΔΨm比值变化相对最轻。结论HI导致的脑细胞线粒体功能降低有短时间恢复的可能,两种动物的ΔΨm改变有不同的时间规律和易损部位,提示针对不同部位的HIBD实验研究采用不同方法制备动物模型的可行性。     

MK-801对围生期缺氧缺血性损伤后脑细胞线粒体膜电势的影响

目的了解围生期缺氧缺血性脑损伤(HIBD)后脑细胞线粒体膜电势(△ψm)的变化及NMDA型谷氨酸受体拮抗剂MK-801对这一变化的影响.方法应用7日龄新生SD大鼠HIBD动物模型,将实验动物分为正常对照组(n=6),HIBD组(n=10)和HIBD+MK-801组(n=10)(MK-801于低氧处理前按0.3mg/kg剂量腹腔注射).于缺氧缺血后立即断头处死动物,制成脑细胞悬液后,以罗丹明123(Rho123)标记、以流式细胞仪测定△ψm的变化.结果围产期HIBD时双侧脑细胞△ψm值均显著降低,差异具有显著性(P＜0.05),以损伤侧(右侧)为甚,右侧脑细胞△ψm由正常状态下的(18.93±0.74)MFL降至损伤后的(7.59±0.32)MFL,右左△ψm比值由正常状态下的1.06±0.05降至损伤后的0.80±0.06(降低了24.5%),差异具有显著性(P＜0.05).结论HIBD后脑细胞△ψm明显降低,提示线粒体功能明显受损;MK-801可减轻这一变化,提示NMDA型谷氨酸受体拮抗剂可通过减轻线粒体功能受损程度治疗围产期缺氧缺血性脑损伤.     

MK-801对围生期缺氧缺血性损伤后脑细胞线粒体膜电势的影响

目的了解围生期缺氧缺血性脑损伤(HIBD)后脑细胞线粒体膜电势(△Ψm)的变化及NMDA型谷氨酸受体拮抗剂MK-801对这一变化的影响。方法应用7日龄新生SD大鼠HIBD动物模型,将实验动物分为正常对照组(n=6),HIBD组(n=10)和HIBD+MK-801组(n=10)(MK-801于低氧处理前按0.3mg/kg剂量腹腔注射)。于缺氧缺血后立即断头处死动物,制成脑细胞悬液后,以罗丹明123(Rho123)标记、以流式细胞仪测定△Ψm的变化。结果围产期HIBD时双侧脑细胞△Ψm值均显著降低,差异具有显著性(P<0.05),以损伤侧(右侧)为甚,右侧脑细胞△Ψm由正常状态下的(18.93±0.74)MFL降至损伤后的(7.59±0.32)MFL,右:左△Ψm比值由正常状态下的1.06±0.05降至损伤后的0.80±0.06(降低了24.5%),差异具有显著性(P<0.05)。结论HIBD后脑细胞△Ψm明显降低,提示线粒体功能明显受损;MK-801可减轻这一变化,提示NMDA型谷氨酸受体拮抗剂可通过减轻线粒体功能受损程度治疗围产期缺氧缺血性脑损伤。     

脑室注射N-苯甲基氧化碳酰-缬氨酸-丙氨酸-天冬氨酸-氯化丙酮对新生鼠缺氧缺血性脑损伤的保护作用

目的研究广谱Caspase抑制剂N-苯甲基氧化碳酰-缬氨酸-丙氨酸-天冬氨酸-氯化丙酮(zVAD-fmk)对新生大鼠缺氧缺血性脑损伤(HIBD)的保护作用。方法将新生7日龄SD大鼠36只随机分为缺氧缺血(HI)对照组(A)、zVAD-fmk治疗组(B)和假手术组(C)。B组动物于HI前即刻脑室注射zVAD-fmk 1μg,A组注射同体积PBS。建立HIBD动物模型,观察HIBD模型大鼠HI后24 h脑含水量及流式细胞术检测海马细胞凋亡百分率1、4 d体质量增长率和脑组织病理变化。结果HI后24 h,B组HIBD新生鼠结扎侧脑组织含水量、海马神经细胞凋亡率较A组明显减少;HI后14 d体质量增长率B组与A组无显著差异;缺血侧皮质、海马神经元死亡率B组较A组明显降低。结论脑室注射zVAD-fmk可减少HIBD后早期和中期神经细胞凋亡,对新生大鼠HIBD具有一定保护作用。     

神经生长因子对缺氧缺血新生大鼠一氧化氮合成酶表达的影响

目的 探讨缺氧缺血(HI)后神经型一氧化氮合酶(nNOS)的变化及神经生长因子(NGF)对新生大鼠缺氧缺血性脑损伤(HIBD)的保护作用.方法 夹闭妊娠足月Wistar大鼠子宫血管,制成HIBD新生鼠模型.治疗组给予腹腔注射NGF4000 U/kg,1次/d,分别用1、3、7次.在生后不同时间检测nNOS表达、NO含量及细胞凋亡数量.结果 治疗组的NO含量明显降低,24 h的NO含量(μmol/L)为23.98±2.37,72 h为22.17±1.74,而HIBD组24 h和72 h的含量分别为31.64±3.23和30.31±1.76,两组比较,差异有统计学意义(P＜0.05);治疗组nNOS的表达也下降,24 h和72 h的表达量(个/mm2)为26.8±0.8和29.2±1.8,而同时间点HIBD组nNOS表达量为54.7±2.2和34.5±1.4,两组比较,差异有统计学意义(P＜0.05);神经细胞凋亡情况,治疗组72 h、7 d皮质和海马区的凋亡细胞数(个/mm2),分别为41.4±1.3、5.6±0.6和43.9±1.8、5.8±1.2,而HIBD组72 h、7 d皮质和海马区的凋亡细胞数分别为51.6±2.5、12.6±1.4和58.7±2.6、15.2±1.7,治疗组的凋亡细胞数明显降低,同时期同部位比较均有统计学意义(P＜0.05).结论 本研究证实NGF对新生大鼠HIBD有保护作用,通过抑制nNOS的表达,降低了炎性细胞因子NO的含量,减轻了HIBD后的脑细胞凋亡,证实NGF抗凋亡作用与抑制nNOS的表达从而减少NO生成有关.     

NMDA受体拮抗剂MK-801对缺氧缺血性脑损伤保护作用的机制探讨(英文)

目的　NMDA型谷氨酸受体的激活在缺氧缺血性脑损伤 (HIBD)的病理生理过程中具有重要的作用。该研究探讨NMDA型谷氨酸受体拮抗剂MK 80 1对HIBD的保护机制。方法　 30只 7日龄SD大鼠随机分为正常对照组、HIBD组和HIBD +MK 80 1组 ,每组 1 0只 ,后两组大鼠结扎右颈总动脉后暴露于低氧环境制备HIBD模型 ,HIBD +MK 80 1组大鼠于低氧处理前腹腔注射MK 80 1 0 .3mg/kg。所有大鼠于HI后立即断头处死 ,制备脑单细胞悬液 ,以流式细胞仪测定脑细胞线粒体跨膜电势 (△Ψm)、以荧光扫描仪测定脑细胞内游离钙([Ca2 + ]i)水平。结果　与正常对照组相比 ,HIBD组大鼠双侧脑细胞△Ψm值及右 :左△Ψm比值均显著降低 ,[Ca2 + ]i显著升高 ,差异均有显著性 (P <0 .0 5或 0 .0 1 ) ;MK 80 1 +HIBD组大鼠脑细胞右 :左侧△Ψm比值较HIBD组升高 ,其差异有显著性 (P <0 .0 5 ) ,但两组间脑细胞右 :左 [Ca2 + ]i的比值无显著性差异 (P >0 .0 5 )。结论　MK 80 1对缺氧缺血性脑损伤的保护作用与其改善脑细胞线粒体功能有关 ,而与其对 [Ca2 + ]i水平的影响关系不大 ,其保护机制可能不是经过“NMDA受体 [Ca2 + ]i △Ψm”途径、而是通过“NMDA受体 其它 △Ψm”途经发挥作用。     

整合素连接激酶在新生鼠缺氧缺血性脑损伤中的表达及作用

目的探讨整合素连接激酶(ILK)/磷酸化蛋白激酶B(Akt)信号通路在新生鼠缺氧缺血性脑损伤(HIBD)修复中的作用。方法采用10日龄SD新生大鼠随机分为假手术组(n=3)和缺氧缺血组(HI组,n=23),建立HIBD模型,于HI后0、4、6、12、24、48、72 h处死取脑,免疫荧光法检测ILK表达与分布,Western blot检测ILK、Akt、磷酸化蛋白激酶B(p-Akt)、血管内皮生长因子(VEGF)的表达情况。构建靶向ILK RNA干扰的慢病毒载体,抑制新生鼠脑组织中ILK的表达。右侧侧脑室分别注射含有LV-ILK shRNA慢病毒(n=15)和LV-control慢病毒对照(n=3),建立HIBD模型,于HI后4 h和24 h处死动物取脑,Western blot检测ILK、Akt、p-Akt、VEGF蛋白的表达变化,TUNEL染色检测细胞凋亡。结果 ILK主要表达于皮层和海马区,定位于胞浆和胞膜,在假手术组和HI组均有表达。ILK于HI后表达开始逐渐增加,24 h达高峰,之后表达有所降低。p-Akt于HI后4 h明显增加,后逐渐降低,24 h降至最低,后又增加,在48 h达高峰。VEGF于HI后4 h表达开始增加,12 h达高峰,后维持较高水平。构建的靶向ILK RNA干扰的慢病毒载体在体内应用获得成功。注射慢病毒LV-ILK shRNA组在HI 4 h、24 h时所表达的ILK、p-Akt、VEGF均明显低于同一时间点的LV-control组,同时细胞凋亡明显增加。结论新生大鼠HIBD后,ILK、p-Akt、VEGF蛋白表达均增高,通过抑制ILK的表达,能够降低新生大鼠HIBD后p-Akt和VEGF蛋白表达,增加细胞凋亡。提示HIBD后可能通过ILK/Akt信号通路,增加VEGF表达,进而促进神经细胞存活及血管再生,在新生鼠HI脑损伤修复中发挥作用。     

缺氧缺血性脑损伤新生大鼠内质网应激相关因子的表达

目的 观察内质网应激相关因子氧调节蛋白150(ORP150)和C/EBP同源蛋白(CHOP)在缺氧缺血性脑损伤(HIBD)新生大鼠脑皮质内的表达,探讨内质网应激在新生大鼠HIBD中的作用.方法 新生7日龄SD大鼠随机分为假手术组和缺氧缺血(HI)组.每组按照观测的时间点不同分为3h、6h、12h、24h、3d、7d6个亚组,每个亚组8只.在每个时间点将大鼠断头后取皮质脑组织匀浆,用Western blot方法检测不同时间点其脑皮质ORP150及CHOP的动态变化.用原位末端标记法检测相应时间点光镜下其脑皮质组织的凋亡细胞数.结果 1.HI组CHOP表达水平在HIBD后各时间点均高于假手术组(P＜0.05),且在24h达到高峰;ORP150表达水平在完成HIBD后3h开始增加,6h达到高峰,后逐渐下降,7d时与假手术组比较差异无统计学意义(P＞0.05).2.HI后3h,HI组即发现结扎侧脑皮质有少量的凋亡细胞,随着HI时间的延长,凋亡细胞逐渐增多,24h达到高峰后下降.3.CHOP的表达变化与神经细胞凋亡时间趋势呈正相关(r=0.911,P＜0.05).结论 HIBD诱发了内质网应激,可能通过上调ORP150表达参与启动末折叠蛋白反应过程,而通过上调CHOP表达诱导神经细胞凋亡的发生.     

神经生长因子对新生大鼠缺氧缺血性脑损伤的保护作用

目的：研究神经生长因子(NGF)对新生大鼠缺氧缺血性脑损伤(HIBD)的保护作用。方法：将新生7日龄SD大鼠40只随机分为NGF治疗组(n=16),对照组(n=16)和假手术组(n=8),缺氧缺血(HI)后即刻腹腔注射100 U NGF或等量生理盐水(假手术组不注射),然后观察NGF对HIBD模型鼠的体重增长、脑组织病理及超微结构改变的影响,并用TUNEL法原位标记DNA片段,观察NGF对HIBD后脑细胞凋亡的影响。结果：NGF治疗组体重增长(4.16±0.24) g明显高于对照组(2.86±0.17) g,(P<0.01);TUNEL检测结果,HIBD后24 h治疗组左侧海马和皮质凋亡细胞数(分别为199.75±19.61,182.75±19.12)明显低于对照组(分别为285.50±32.67,271.00±28.36)(P<0.01);HIBD后48 h治疗组左侧海马、皮质凋亡细胞数(分别为77.75±15.76,82.50±19.15)亦明显低于对照组(分别为106.50±16.96,122.75±16.56)(P<0.01)。结论：外源性NGF对HIBD后脑细胞凋亡可能具有一定的保护作用。     

促红细胞生成素对缺氧缺血新生鼠脑匀浆一氧化氮及血浆内皮素的影响

目的探讨体外注射重组人促红细胞生成素(rhEPO)对新生鼠缺氧缺血后脑组织一氧化氮(NO)和NO合成酶(NOS)及血浆内皮素(ET)水平的影响,阐明其对缺氧缺血(HI)新生动物神经保护作用的机制。方法将7日龄SD大鼠制备缺氧缺血脑损伤(HIBD)模型及rhEPO治疗模型,将假手术组作对照。测定各组新生鼠HI后6 h脑组织匀浆NO和NOS含量以及血浆ET水平。结果HIBD组在HI后6 h脑组织NO、NOS及血浆ET均升高(P<0.05),rhEPO组脑组织NO、NOS显著降低水平(P<0.05),而血浆ET含量无明显改变。结论外源性rhEPO可通过减少NO的过量生成而对HIBD后的脑组织起到保护作用。     

Allergic factors associated with the development of asthma and the influence of cetirizine in a double-blind, randomised, placebo-controlled trial: First results of ETA®

There is a common progression known as the allergic march from atopic dermatitis to allergic asthma. Cetirizine has several antiallergic properties that suggest a potential effect on the development of airway inflammation and asthma in infants with atopic dermatitis. Methods. Over a two year period, 817 infants aged one to two years who suffered from atopic dermatitis and with a history of atopic disease in a parent or sibling were included in the ETAC^® (Early Treatment of the Atopic Child) trial, a multi-country, double-blind, randomised, placebo-controlled trial. The infants were treated for 18 months with either cetirizine (0.25mg/ kg b.i.d.) or placebo. The number of infants who developed asthma was compared between the two groups. Clinical and biological assessments including analysis of total and specific IgE antibodies were performed. Results. In the placebo group, the relative risk (RR) for developing asthma was elevated in patients with a raised level of total IgE (≥ 30 kU/I) or specific IgE (≥ 0.35 kUA/I) for grass pollen, house dust mite or cat dander (RR between 1.4 and 1.7). Compared to placebo, cetirizine significantly reduced the incidence of asthma for patients sensitised to grass pollen (RR = 0.5) or to house dust mite (RR = 0.6). However, in the population that included all infants with normal and elevated total or specific IgE (intention-to-treat - ITT), there was no difference between the numbers of infants developing asthma while receiving cetirizine or placebo. The adverse events profile was similar in the two treatment groups. Discussion. Raised total IgE level and raised specific IgE levels to grass pollen, house dust mite or cat dander were predictive of subsequent asthma. Cetirizine halved the number of patients developing asthma in the subgroups sensitised to grass pollen or house dust mite (i.e. 20% of the study population). In view of the proven safety of the drug, we propose this treatment as a primary pharmacological intervention strategy to prevent the development of asthma in specifically sensitised infants with atopic dermatitis.     

Resurgence of measles in Singapore: profile of hospital cases

OBJECTIVE: To ascertain the profile of cases of measles seen at a general hospital during a recent outbreak that occurred despite a measles vaccination program. METHODOLOGY: A retrospective study from January 1991 to March 1998. All patients with measles (ICD code 055. 9) seen at the emergency unit or as inpatients were included. RESULTS: There were 87 cases identified. The diagnosis was clinical in all and proven serologically in 71%. Eighty-five per cent of the cases occurred between January 1997 and March 1998. There was a bi-modal age distribution with peaks in the very young (相似文献   

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孤独症谱系障碍(autistic-spectrum disorders,ASDs)近年来患病率逐年攀升至1%左右,其症状往往伴随终生,成为严重威胁儿童健康和发展的神经发育性疾患;注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)是儿童期最常见的精神障碍,国内报道患病率为4.13%～5.83%,其症状可延续至青少年期,甚至到成年期[1]。这两类精神障碍在成年期的临床表现、共患病、治疗策略和预后与儿童期有哪些不同呢?本文通过回顾相     

EXCITING NEW TREATMENT APPROACHES FOR PATHYPHYSIOLOGIC MECHANISMS OF SICKLE CELL DISEASE

During the past several decades, our understanding of the complex pathophysiology of vasoocclusion associated with sickle cell disease has improved greatly. Interaction of genes, hemoglobin molecules, red cell membrane and metabolic changes, cell-cell interactions and cell-plasma interactions, red cell adhesion to vascular endothelium, activation of coagulation, and vascular reactivity play a role in vaso occlusion. Penicillin prophylaxis of pneumococcal infections and appropriate use of blood transfusions and other supportive measures improved survival of sickle cell patients. Hydroxyurea made a major impact on sickle cell therapy when it was shown to decrease acute painful episodes, acute chest syndrome, and the need for blood transfusion in adults. Significant experience in the use of hydroxyurea has been accumulated in older children. The benefits and risks of hydroxyurea for younger children and long-term risks in all patients will be evaluated in future investigations. Other promising therapies include butyrate compounds, clotrimazole, magnesium supplementation, poloxamer 188, antiadhesion agents, anticoagulant approaches, and nitric oxide. Hemopoietic transplantation remains the only curative therapy. However, several transgenic mouse models are available for studies of gene therapy or other treatment approaches on biochemical, cellular, and pathologic effects of mutant genes.     

Infiltrations of Epstein-Barr virus-carrying cells in granular lymphocyte-proliferative disorders corresponding to chronic active Epstein-Barr virus infection

A 21-year-old man with granular lymphocyte-proliferative disorders (GLPD) associated with chronic active Epstein-Barr virus (EBV) infection is described. Chromosomal analyses revealed several clonal abnormalities and two of them were mainly repetitious. High copy numbers of monoclonal EBV genome were also detected in the proliferative large granular lymphocytes (LGLs), indicating the monoclonal expansion of EBV-infected LGLs. The patient had an indolent course for several years, and there was no evidence of infiltrations of his bone marrow until the end stage. At autopsy, microscopic studies revealed marked infiltrations of LGL in the liver and spleen, and the infiltrating cells were NK-cell immunophenotype. The infiltrated LGLs showed latency I.     

LUTEINIZING HORMONE RECEPTOR MUTATIONS IN DISORDERS OF SEXUAL DEVELOPMENT AND CANCER

Human male sexual development is regulated by chorionic gonadotropin (CG) and luteinizing hormone (LH). Aberrant sexual development caused by both activating and inactivating mutations of the human luteinizing hormone receptor (LHR) have been described. All known activating mutations of the LHR are missense mutations caused by single base substitution. The most common activating mutation is the replacement of Asp-578 by Gly due to the substitution of A by G at nucleotide position 1733. All activating mutations are present in exon 11 which encodes the transmembrane domain of the receptor. Constitutive activity of the LHR causes LH releasing hormone-independent precocious puberty in boys and the autosomal dominant disorder familial male-limited precocious puberty (FMPP). Both germline and somatic activating mutations of the LHR have been found in patients with testicular tumors. Activating mutations have no effect on females. The molecular genetics of the inactivating mutations of the LHR are more variable and include single base substitution, partial gene deletion, and insertion. These mutations are not localized and are present in both the extracellular and transmembrane domain of the receptor. Inactivation of the LHR gives rise to the autosomal recessive disorder Leydig cell hypoplasia (LCH) and male hypogonadism or male pseudohermaphroditism. Severity of the clinical phenotype in LCH patients correlates with the amount of residual activity of the mutated receptor. Females are less affected by inactivating mutation of the LHR. Symptoms caused by homozygous inactivating mutation of the LHR include polycystic ovaries and primary amenorrhea.     

A profile of respiratory symptoms in urban and rural South Australian school children

This report describes the cross-sectional analyses of data from the first year of a longitudinal study using questionnaire and respiratory function data over a 5 year period from a sample of rural South Australian school children. The cumulative or lifetime prevalences of respiratory symptoms were estimated in 825 rural and 1261 urban school children aged between 5 and 15 years in order to determine if the prevalence rates differed between rural and urban school children. The study found the overall cumulative prevalence of asthma and/or wheezy breathing (AWB) to be 24.1% in the rural school children compared to 27.6% in the urban school children. Most children developed AWB symptoms before the age of 7 years, with 20% reporting moderately severe symptoms and 10% having more than one attack per fortnight. The cumulative prevalence of bronchitis, loose/rattly cough (BLRC) differed significantly between the rural school children (34.1%) and urban school children (47.9%). The BLRC symptoms preceded the development of AWB in many cases. Urban school children also reported a higher prevalence of atopic conditions.     

Personality profiles and heart rate variability (vagal tone) in children with recurrent abdominal pain

The aim of the study was to explore psychological factors and autonomic activity in children with recurrent abdominal pain and to compare them with those in a control group of healthy children. The Personality Inventory for Children was used for assessment of developmental, emotional and psychosocial factors in 25 children with recurrent abdominal pain (age, 7-15 y). Parasympathetic and sympathetic functions in these children and in 23 healthy control subjects (age, 7-13 y) were also investigated, non-invasively using a computerized polygraph. Vagal tone (parasympathetic function) was indexed by calculation of respiratory sinus arrhythmia in beats/min. Skin conductance (sympathetic function) was recorded by the constant current method. On the Personality Inventory for Children, 16 patients had high scores on somatic concern. Several patients had scores in the clinical range for depression, withdrawal and anxiety, but the mean scores for these personality profile scales were well within the normal range of healthy children. Interestingly, there was a spike on the L (Lie)-scale for most of the patients and 15 patients had scores above or close to the clinical cut-off value. As compared with the scores in healthy children, vagal tone and sympathetic tone were normal. Conclusion: Many children with recurrent abdominal pain have scores in the clinical range for depression, withdrawal, anxiety and L-scale indicating coping problems, denial and a trend towards somatic concern that may contribute to the evolution of abdominal pain. Autonomic nerve activity was not disturbed in these children.     

Hauttemperaturen verschiedener Körperoberflächenareale des Rumpfes bei Säuglingen

Summary In two groups of infants (3–53 weeks old) skin temperatures were controlled in different areas of the trunk—i.e.: regions of sternum, lungs, heart, liver, spleen, kidneys—at different room-temperatures (group I: 21–25°C; group II: 29–32°C). Rectal temperatures of some probands in both groups also had been controlled simultaneously. A definite change in the reaction to heat was proofed in different periods of the first year of life. In higher environmental temperatures the skin temperature was almost constant at every controll-point of the skin, even in older infants. In lower environmental temperatures the skin temperatures lowered continuously with age till 7. to 9. moth. From 10. to 12. month the lowering of skin temperature discontinued. The rectal temperatures were relatively constant in all infants. Only in infants from 7. to 12. month, whose skin temperatures were controlled in lower as well as in higher environmental temperatures, a tendency to higher rectal temperatures was proofed in warmer environmental temperatures.The significance of these results is discussed.

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Untersuchungen mit Unterstützung durch die Deutsche Forschungsgemeinschaft.