GLP-2改善短肠综合征大鼠残留小肠平滑肌运动功能的实验研究

目的 了解短肠综合征大鼠残存小肠自发性节律性收缩运动及卡巴胆碱诱导小肠平滑肌肌条收缩反应的变化趋势,并探讨腹腔注射胰高血糖素多肽-2 (GLP-2)对短肠综合征大鼠残存小肠术后代偿反应的改善作用及其机制.方法 通过外科手术方法建立动物模型,40只SD大鼠随机分成4组分别为假手术组(设为对照组)、SBS1W组、SBS2W组、G-SBS1W组,G-SBS1W组腹腔注射125μg·kg-1·d-1的GLP-2溶液(20μg/ml),每天2次,连续5d.苏木精-伊红(HE)染色研究小肠全壁形态学改变；电镜观察黏膜上皮及平滑肌细胞的超微结构改变；环形平滑肌肌条实验研究其自发性节律性收缩变化规律及卡巴胆碱诱导肌条收缩反应的变化趋势.结果 短肠综合征大鼠术后1周残存小肠肠管显著扩张；HE染色显示SBS1W组大鼠小肠黏膜上皮增生明显,平滑肌层肥厚、平滑肌增生；环形平滑肌肌条实验提示平滑肌自发性节律性收缩紊乱、幅度不规则、频率变慢；短肠综合征大鼠术后1周卡巴胆碱诱导肌条收缩反应明显增强,术后2周后基本恢复假手术组水平；G-SBS1W组术后1周黏膜上皮进一步代偿,而平滑肌肥厚、增生不明显,环形平滑肌肌条实验及卡巴胆碱反应曲线与假手术组相似.结论 短肠综合征大鼠术后1周残存小肠动力发生动力改变,GLP-2能明显改善短肠综合征大鼠残存小肠的形态及功能.     

维生素D调节坏死性小肠结肠炎新生大鼠肠道上皮occludin蛋白表达的研究

目的：检测坏死性小肠结肠炎(necrotizing enterocolitis,NEC)新生大鼠肠道上皮occludin蛋白的定位及表达情况,探索维生素D处理对NEC新生大鼠的保护作用及对occludin蛋白表达的影响。方法 SPF级不同窝别新生48 h的Wistar大鼠60只,采用随机数字表法随机分为4组：母乳喂养＋对照组10只,母乳喂养＋维生素D组10只,NEC＋对照组20只,NEC＋维生素D组20只。 NEC模型：将生后48 h的仔鼠与母鼠隔离,采用鼠乳代乳品人工喂养＋缺氧＋寒冷刺激处理;维生素D处理：分别于NEC造模前30 min,造模后1 d、2 d腹腔注射活性维生素D(帕立骨化醇)。各组大鼠分别在实验72 h后处死取材,选取回肠组织采用HE染色观察肠腔结构改变并做Nadler病理评分,采用免疫荧光染色观察occludin蛋白在肠上皮的定位和表达情况,采用Western blot方法检测肠道黏膜组织occludin蛋白的表达量并做统计学分析。结果 HE染色可见NEC大鼠的肠腔组织结构破坏,黏膜下或肌层分离,部分绒毛脱落,甚至肠绒毛消失,肠上皮脱落伴肠坏死,Nadler病理评分为(2.90±0.23)分;维生素D处理的NEC大鼠上述病理表现较NEC大鼠减轻,Nadler病理评分为(1.70±0.21)分,两者比较差异有统计学意义(P<0.01)。免疫荧光显示NEC大鼠肠道上皮细胞间occludin表达明显减少、稀疏,呈现不连续或点状表达,维生素D处理的NEC大鼠肠道上皮细胞间occludin表达较NEC对照组大鼠明显增多,基本呈均匀、连续的表达。 Western blot显示NEC大鼠肠道黏膜组织的occludin表达明显减少,维生素D处理可以明显增加 occludin的表达( P <0.01)。结论 NEC 模型大鼠肠道上皮紧密连接相关蛋白occludin表达明显降低,维生素D处理可以通过上调肠道上皮occludin的表达来抑制NEC的发生发展。     

应用猪小肠黏膜下层进行兔尿道缺损修补的研究

目的 探讨应用异种猪小肠黏膜下层无细胞基质补片进行尿道缺损修复的可行性方法.方法 小肠黏膜下层无细胞基质(SIS)取自健康处死的猪,经过组织学处理,并经HE及Masson's染色分析后,用于兔尿道缺损的修复治疗.12只成年雄性新西兰白兔建立尿道部分缺损模型;分2组各6只,一组应用SIS进行修复治疗,另一组单纯缝合作对照;术后4和12周各组分别处死3只,对再生的尿道组织行组织学和免疫组化检测;术后12周行逆行尿道造影用于评价尿道的开放功能.结果 治疗组术后4周可见尿路上皮自吻合口两侧迁入并完全覆盖尿道内腔,基质中可见少量新生血管和平滑肌细胞,基质和吻合口部位可有少量炎性细胞浸润;术后12周.再生组织与尿道形态几乎无异,尿道造影显示无明显尿道狭窄.而对照组均出现尿道狭窄.结论 猪小肠黏膜下层对于兔尿道损伤的修复是一种有用的材料,该基质制作简单,在尿道的结构和功能重建方面具有良好的特性.     

坏死性小肠结肠炎新生大鼠核因子-κB活性变化及肠三叶因子的干预作用

目的 研究肠三叶因子(ITF)对坏死性小肠结肠炎(NEC)新生大鼠肠黏膜组织核因子-κB(NF-κB)表达的影响,探讨ITF是否对NEC具有保护作用及其在NEC发病机制中的作用.方法 新生鼠50只随机分为5组,每组10只,A组(正常对照组)不做处理;B组(ITF组)皮下注射ITF 0.2 mg;C组为NEC模型组;D组[NEC加9g/L盐水(NS)组]制备NEC模型后皮下注射NS;E组(NEC加ITF组)制备NEC模型后皮下注射ITF 0.2 mg,连续3 d.大鼠均于实验第4天处死.分别于其十二指肠、小肠近中远端及结肠近端和远端处取1～2 cm肠道组织固定、包埋、切片、HE染色行病理学检查及免疫组织化学染色观察NF-κB表达.结果 C、D组组织中NF-κB(p65)阳性表达较A、B及E组显著升高(Pa ＜0.01),E组与A、B组比较也有升高(Pa ＜0.01),且随NF-κB(p165)的激活有明显的核转移;病理切片示C、D组HE染色见肠肇损伤轻重不一,可见全肠黏膜绒毛坏死,病理评分2～4分;E组轻度肠上皮细胞脱落,顶端绒毛坏死,肠组织病理评分0～2分.结论 通过皮下注射ITF可减轻NEC新生大鼠肠道炎性反应,NF-κB通路参与了NEC的发病过程,ITF可能通过抑制NF-κB的活化保护NEC模型新生大鼠的肠黏膜.     

胰高血糖素样肽-2对小鼠肠黏膜干细胞LGR5表达的影响及对肠道黏膜的保护作用

目的 研究LGR5肠道干细胞在内毒素血症肠黏膜损伤修复中的作用,是否可以通过调节干细胞的增殖分化来促进肠黏膜的修复.方法 21日龄健康Wistar幼鼠,随机分成对照组、脂多糖（lipopolysaccharide,LPS）组和胰高血糖素样肽-2（glucagon-like peptides 2,GLP-2）组.LPS组及GLP-2组腹腔注射LPS 5 mg/kg,GLP-2组腹腔注射LPS 1 h后腹腔注射GLP-2 250 μg/kg;对照组腹腔注射生理盐水1 ml/kg;在LPS注射后6h、24 h及72 h取末端回肠.光镜及电镜观察各组回肠上皮结构改变,免疫组织化学、RT-PCR方法检测肠道干细胞标记物LGR5的表达.结果 LPS注射后6h,LPS组及GLP-2组大体可见肠管充血、水肿.光镜下可见绒毛断裂、倒伏,炎性细胞浸润,腔内可见渗出液,24h及72h LPS组及GLP-2组肠黏膜损伤逐渐修复,绒毛逐渐生长,GLP-2组较LPS组修复明显,72h GLP-2组上皮基本恢复正常.免疫组织化学可见LGR5抗体标记在隐窝内,LPS组及GLP-2组在绒毛底部及绒毛处可见LGR5抗体标记,GLP-2组表达多于LPS组.RT-PCR检测,LPS组LGR5 mRNA表达6 h（0.13±0.05）、24h（0.16±0.05）、72 h（0.16±0.04）均明显高于对照组（0.12 ±0.03）,差异均有统计学意义（P均＜0.05）;GLP-2组LGR5 mRNA表达6h（0.52±0.09）、24 h（0.73 ±0.14）、72 h（0.48 ±0.24）,明显高于LPS组,差异均有统计学意义（P均＜0.05）.结论 内毒素血症肠上皮黏膜炎症损伤后,肠上皮干细胞增殖分化,可能参与修复炎症损伤后的肠黏膜;外源性给予GLP-2可促进内毒素血症肠黏膜损伤的修复.     

早期营养干预对宫内生长迟缓大鼠胰岛素样生长因子和小肠发育及生长追赶的影响

目的　探讨早期营养干预对宫内生长迟缓 (IUGR)幼鼠血清胰岛素样生长因子 (IGF)和小肠发育及生长追赶的影响。方法　将 2 4只IUGR新生雌鼠和 8只正常新生雌鼠随机分为 4组 :IUGR模型组 ,IUGR低蛋白组 ,IUGR高蛋白组 ,正常对照组。于生后 4周时检测各组大鼠血清IGF1、胰岛素样生长因子结合蛋白 3(IGFBP3)浓度、体重、身长和小肠重量、长度及肠黏膜组织结构变化。结果　 4周时IUGR高蛋白组血IGF1、IGFBP3和小肠黏膜绒毛高度、吸收表面积均显著高于对照组和IUGR模型组 (P <0 .0 5或P <0 .0 1) ;小肠重量、长度和体重、身长与对照组比较无显著性差异 (P均 >0 .0 5 )。结论　生后头 4周予高蛋白饮食早期营养干预IUGR幼鼠 ,可通过促进小肠发育达到满意的体格生长追赶。血清IGF1是反映生长追赶的灵敏指标     

幼年大鼠内毒素血症时小肠上皮细胞凋亡及Caspase-3的表达

目的：儿科危重症中胃肠功能障碍的常见病因是严重感染,其发病机制与内毒素血症导致肠黏膜屏障功能破坏密切相关。该研究探讨幼年大鼠内毒素血症时肠黏膜屏障损伤的细胞凋亡情况及其可能的信号转导通路,为寻求新的治疗途径提供依据。方法：40只18日龄Wstar大鼠腹腔注射4mg/kg内毒素(大肠杆菌O55∶B5脂多糖1mg/mL)制成内毒素血症模型,对照组大鼠(n=40)腹腔注射1mL/kg生理盐水。两组分别在注射后2, 4, 6, 24, 72h处死8只大鼠,取4cm远端回肠,行苏木精伊红染色,光镜下观察小肠绒毛的病理变化,原位末端标记法(TUNEL)检测小肠上皮的细胞凋亡,免疫组织化学测定Caspase 3的表达。结果：光镜下对照组各时点小肠绒毛结构正常,内毒素组注射后4 ~ 72h可见少量炎症细胞浸润。注内毒素后2h上皮细胞凋亡和Caspase 3的表达明显增加,分别于24h和6h达高峰, 72h开始下降。内毒素组各时间点小肠绒毛上皮细胞凋亡指数和Caspase 3的表达均明显高于对照组,差异有显著性意义(P<0.01或P<0. 001)。结论：幼年大鼠内毒素血症时小肠上皮细胞凋亡增加,Caspase 3表达是其信号转导途径之一。细胞凋亡可能是严重感染时肠黏膜屏障破坏机制。     

肠三叶因子对坏死性小肠结肠炎新生鼠白细胞介素-6的影响

目的探讨肠三叶因子（ITF）对坏死性小肠结肠炎（NEC）新生大鼠肠黏膜组织IL-6水平的影响，分析ITF对NEC的保护作用机制。方法新生鼠32只随机分为4组，每组各8只，正常对照组（A组）；NEC模型组（B组）；NEC模型后予以皮下注射9g/L盐水0．2mL（C组）；NEC模型后予以皮下注射ITF0.2mg（D组）。取近回盲部1-2cm肠道组织固定包埋、切片、HE染色做病理学检查，其他肠道组织制备组织匀浆取上清液检测IL-6水平。结果B、C组组织匀浆IL-6的水平较A、D组显著增高（Pa〈0.05，0．01），A与D组无明显差异（P〉0．05）。病理切片显示C、D组HE染色切片见肠壁损伤轻重不一，可见全肠黏膜绒毛坏死，病理评分的中位积分为3分；D组肠上皮细胞少量脱落，顶端绒毛坏死，病理评分的中位积分为1分。结论通过皮下注射ITF可减轻NEC后的肠道炎性反应。ITF有可能为治疗NEC提供新的方法。     

动物体外构建初级组织工程化血管、体内强化的实验研究

目的 采用在动物体外构建初级组织工程化血管、体内强化的方法 ,探讨组织工程技术构建组织工程化血管的可能性.方法 5-溴-2-脱氧尿嘧啶核苷(Brdu)标记所有种子细胞,4,6-二脒基-2-苯基吲哚(DAPI)标记内皮样细胞,观察细胞标记的成功率;血管平滑肌样细胞(VSMLCs)和血管内皮样细胞(VELCs)分层种植于胶原包埋聚乙醇酸(PGA)的复合支架表面;将细胞和支架的复全体种植于动物皮下,并设立对照组,分别于植入后的第4,6、8周再次麻醉动物,取出植入皮下的组织工程化血管,行组织学及免疫荧光等检查.结果 组织学观察实验组管壁结构比较清晰,细胞数量也已减少,胶原成分增多,管壁分层明显,可见内膜、中膜和外膜,对照组无此特点;实验组皮下培养8周Brdu标记细胞的免疫荧光观察见部分细胞核呈现明亮的黄绿色荧光,证明来源于所种植的种子细胞.结论 体外构建的初级组织工程化血管,以动物的皮下为生物反应器,采用静态培养的方式可使血管壁得以强化,从而构建出次级组织工程化血管;组织工程技术构建的次级工程化血管组织其大体结构与天然血管相似;血管壁细胞有种植的种子细胞生长,并参与了.组织工程化血管的重构.     

谷氨酰胺对新生鼠坏死性小肠结肠炎的影响

目的探讨谷氨酰胺(glutamine,Gln)对新生鼠坏死性小肠结肠炎(necrotizing enterocoli-tis,NEC)肠黏膜修复的影响。方法新生1日龄Wistar大鼠30只随机分为三组,A组为正常对照组;B组为NEC模型组;C组为NEC模型后灌胃给Gln组(2·0g/kg·d)。建立NEC模型,连续3天给予新生鼠100%二氧化碳5min,然后再给予100%氧气5min,放回母鼠身边喂养,第4天断头处死新生鼠,取肠道组织待检。分别取近回盲段2~3cm肠道组织固定、包埋、切片。HE染色光镜下作病理学检查,应用免疫组化技术检测肠黏膜增殖细胞核抗原(PCNA)表达情况,原位末端标记(TUNEL)法检测肠黏膜细胞凋亡的变化。结果B组HE染色切片见肠壁有不同程度的损伤,病理评分的中位积分为3分;C组有的肠黏膜正常,有的轻度肠上皮细胞脱落,有的绒毛轻度坏死,病理评分的中位积分为1分。B组PCNA数量均低于A组及C组(P<0·01)。B组的肠黏膜细胞凋亡的数量高于A组及C组(P<0·01)。结论NEC时,新生鼠肠黏膜受损,增殖减慢,细胞凋亡的数量增加;补充Gln可促进NEC新生鼠肠黏膜隐窝细胞增殖,减少肠黏膜细胞凋亡数量,使肠黏膜修复加快。     

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.