Biting attack elicited by stimulation of the ventral midbrain tegmentum of cats

An area in the ventral midbrain tegmentum has been discovered in which electrical stimulation elicits biting attack. The midbrain sites from which attack was elicited correspond well with the zone in the midbrain tegmentum where degeneration was previously observed after lesions were made in lateral hypothalamic attack sites.     

Neural pathways from thalamus associated with regulation of aggressive behavior

Small electrolytic lesions were made through electrodes in the thalamus of cats at sites where electrical stimulation elicited attack on a rat. Staining by modified Nauta reduced silver methods revealed that significant degeneration passed caudally from the lesions and entered the midbrain dorsal central gray region. Electrical stimulation of this dorsal midbrain region elicited attack on a rat, and destruction of this region suppressed the attack elicited by thalamic stimulation.     

稚鳖粘液性肠炎病的病理形态学研究

稚鳖粘液性肠炎病的主要眼观病变是病鳖肛门排出粘液块,组织病理变化主要为肠腺分泌亢进,肠上皮细胞脱落,肠壁充血,肝脏脂肪变性,脾脏炎性细胞浸润,肾脏肾小管上皮细胞水泡变性,肺也有不同程度的病变。电镜下观察,发现随着病程的延续肠道的病变相应地加重,主要表现为炎性细胞浸润,上皮细胞变性和坏死。     

Superior colliculus of the tree shrew: a structural and functional subdivision into superficial and deep layers

Superficial lesions of the superior colliculus produced deficits in form discrimination, while deeper lesions produced, in addition, an inability to track objects. These two syndromes were related to an anatomical subdivision: Superficial lesions resulted in anterograde degeneration in the visual thalamus, whereas lesions confined to the deeper layers produced degeneration in the nonvisual thalamus and in brainstem motor areas.     

不同营养条件下氟对小鼠肝肾及心肌的影响

将64只昆明鼠分为4组,分别给以0,25,50,100mgF／L的饮水,每组动物再分为两小组,设一个低营养组,一个高营养组,以比较相同饮水氟于不同营养条件下肝、肾及心肌的损伤情况。结果表明,在给氟90d时,50及100mgF／L组动物的肝脏可见脂肪及水泡变性,肾脏皮质肾小管上皮可见水泡变性,心肌纤维着色不匀,个别纤维可见颗粒变性。相同氟水平下不同营养组间比较,高营养组上述变化明显减轻,表明补充营养可以缓减氟对软组织的损伤。     

池塘养殖锦鲤体表溃疡病的组织病理学观察

为临床诊断和防治锦鲤Cyprinus carpio koi皮肤溃疡病,采用病理解剖方法对患病锦鲤进行临床观察和组织病理学分析,试验用患病锦鲤取自上海市朝阳锦鲤养殖场发病池塘,确定病鱼10尾(编号1~10),取每条病鱼的组织进行病理解剖、石蜡切片、H-E染色。结果表明:患病锦鲤体表溃疡病处的病灶组织出现严重淤血、炎性细胞浸润并聚集、肌束溶解和坏死等典型病理表现;体表溃疡病是由致病菌局部感染所致,并未全身性感染,10尾病料的脾组织均表现出血管扩张、管壁增厚、血管周围的实质组织凝固变性,伴有红细胞坏死和凝固变性区域内部分组织坏死等较为一致的病理特征,可以诊断为血液中有毒物质引起的脾组织病变,导致脾功能低下;肝胰组织和肾组织较脾组织病变相对较轻;肠、心、鳃、头肾组织等基本正常。研究表明,本病例全部样品均有不同程度的脾凝固变性、肝组织淤血、肾组织间质充血及其组织中血管扩张、管壁增厚的病理变化,这与体表溃疡病变无直接关联。     

Coronary Disease in Spawning Steelhead Trout Salmo gairdnerii

Coronary degeneration was absent in young trout taken in fresh water and rare in immature fish at sea, but the incidence and severity were sharply greater in migrating fish and almost uniformly present in spawning fish. Several fish taken after they had reentered salt water after spawning had no lesions; lesions in fish taken during their second spawning migration were not cumulative. These facts suggest that the process is reversible.     

朱鹮胃瘤线虫病的病理学观察

对 2例朱鹮死亡病例进行了系统的病理学观察。主要肉眼变化为肝、肾、脾肿大 ,腺胃表面有血红色瘤状突起 ,主要组织变化为肝变性、淤血 ,肾变性、坏死、出血 ,腺胃浆膜下有大量虫卵、虫体 ,粘膜上皮细胞坏死 ,间质出血 ,嗜酸性白细胞浸润。同时对雏鸟寄生虫病的危害进行了探讨     

Delayed transneuronal death of substantia nigra neurons prevented by gamma-aminobutyric acid agonist

In an investigation of the mechanism by which brain lesions result in delayed degeneration of neurons remote from the site of injury, neurons within the caudate nucleus of rats were destroyed by local injection of the excitotoxin ibotenic acid. Treatment resulted in the rapid degeneration of the striatonigral pathway including projections containing the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) and delayed transneuronal death of neurons in the substantia nigra pars reticulata. The distribution of nigral cell loss corresponded to the loss of GABAergic terminals. Neuronal death was prevented by long-term intraventricular infusion of the GABA agonist muscimol. Delayed transneuronal degeneration may be produced by neuronal disinhibition consequent to loss of inhibitory inputs. Replacement of inhibitory transmitters by suitable drugs may prevent some forms of delayed neuronal death.     

Amygdaloid nucleus: new afferent input from the vomeronasal organ

Terminal degeneration stained by the Fink-Heimer technique was found in the medial and cortical amygdaloid nuclei in a discrete zone after lesions were inflicted in the accessory olfactory bulb but not after lesions were made in the main olfactory bulb in the rabbit. Since the accessory olfactory bulb receives the endings of the vomeronasal nerve, the mediocortical complex of the amygdala is the central projection area for the vomeronasal sensory organ. The vomeronasal organ is seen as having new potential significance in sexual and feeding behavior because the cortical amygdaloid nucleus projects to the anterior, medial hypothalamus and the ventromedial nucleus.     

Quiet Zone Within a Seismic Gap near Western Nicaragua: Possible Location of a Future Large Earthquake

A 5700-square-kilometer quiet zone occurs in the midst of the locations of more than 4000 earthquakes off the Pacific coast of Nicaragua. The region is indicated by the seismic gap technique to be a likely location for an earthquake of magnitude larger than 7. The quiet zone has existed since at least 1950; the last large earthquake originating from this area occurred in 1898 and was of magnitude 7.5. A rough estimate indicates that the magnitude of an earthquake rupturing the entire quiet zone could be as large as that of the 1898 event. It is not yet possible to forecast a time frame for the occurrence of such an earthquake in the quiet zone.     

七彩山鸡霍乱的病理形态学观察

本文对多杀性巴氏杆菌引起的山鸡霍乱自然病例作了系统的病理形态学观察。眼观病变主要表现为肝脾肿大、表面布有多量灰白色或灰黄色坏死点，肺脏郁血水肿，十二指肠粘膜肿胀充血出血；镜下变化呈急性实质性肝炎、急性坏死性脾炎、出血性和卡他性十二指肠炎、肺脏郁血众肿、肾脏变性与灶性凝固性坏死以及心脏充血和心肌纤维颗粒变性，并在病变器官组织中出现大量细菌或细菌性栓子。上述病变可作为诊断山鸡霍乱的病理学依据。文中还探讨了发病机理，并与家禽霍乱的病变特点作了比较。     

食用动物肝脏的病理学研究

对取自当前广州市肉品市场供食用的２００例猪肝和１００例牛肝的卫生品质进行了病理学分析，发现所研究的６８５猪肝和７７％牛肝存在着各种各样的病变。病变的种类多达２７种。病变不仅有肝细胞的萎缩和各种变性，水肿，囊肿，出血，坏死和钙化肝组织细菌性污染和寄生虫虫卵附着等，还发现恶性肿瘤以及见于癌前期或癌症的肝细胞病理性核有丝分裂像。     

试验感染鸭病毒性肝炎雏鸭的组织病理学研究

对试验感染Ⅰ型鸭肝炎病毒雏鸭的组织病理变化进行了观察,结果表明：接毒后１２ｈ肝、脾、肾及胰等器官组织主要表现为变性性变化;接毒后２４ｈ,则呈现明显的坏死性变化;接毒后７２ｈ及１６８ｈ,则出现较为明显的增生性反应。脑表现为非化脓性脑炎变化。肝、肾、脾及胰的超微结构研究表明,主要是组织细胞的膜系统及核结构的损伤。在肝细胞和脾细胞中有脂滴。在肾小管上皮细胞胞浆中有晶格状排列的类病毒颗粒。     

雏鸡脑脊髓炎病理学观察

对19例自然感染禽脑脊髓炎病毒的发病雏鸡大脑、小脑、脊髓、肝脏、脾脏、胰腺、心脏、肺脏、肾脏、腺胃、肌胃、小肠12种器官进行了病理学观察.结果表明,发病鸡的眼观变化主要为脑膜及切面的出血点和腺胃壁灰白色病灶,其它器官均未有可见病变.显微结构则表现为急性非化脓性脑炎和腺胃淋巴细胞增生的变化:脑实质出血,血管周围淋巴细胞浸润形成管套,神经组织细胞变性、坏死并形成小软化灶,小胶质细胞增生集聚于软化灶;脊髓的背侧和腹侧神经元不同程度变性、坏死;腺胃淋巴细胞增生主要见于腺胃固有层深部复管腺间质中;其它器官仅出现轻度的变性变化.     

Biological bases of childhood shyness

The initial behavioral reaction to unfamiliar events is a distinctive source of intraspecific variation in humans and other animals. Two longitudinal studies of 2-year-old children who were extreme in the display of either behavioral restraint or spontaneity in unfamiliar contexts revealed that by 7 years of age a majority of the restrained group were quiet and socially avoidant with unfamiliar children and adults whereas a majority of the more spontaneous children were talkative and interactive. The group differences in peripheral physiological reactions suggest that inherited variation in the threshold of arousal in selected limbic sites may contribute to shyness in childhood and even extreme degrees of social avoidance in adults.     

野鸭霍乱的病理学观察

本文报告了野鸭霍乱的病理学观察结果。眼观病变主要为肝脾表面散在多量灰白色或灰黄色坏死点，心外膜出血，肺脏部血水肿，十二指肠粘膜肿胀充血出血，全身浆膜出血;镜下变化是肝脏变性坏死、急性脾炎、心外膜出血及心肌纤维颗粒变性、肺脏郁血水肿、出血性和卡他性十二指肠炎，并在肝脾、十二指肠中出现大量细菌或细菌性栓子。病原分高鉴定结果为多杀性巴氏杆菌A型。文中还探讨了发病机理。     

Uncoupling of leading- and lagging-strand DNA replication during lesion bypass in vivo

Numerous agents attack DNA, forming lesions that impair normal replication. Specialized DNA polymerases transiently replace the replicative polymerase and copy past lesions, thus generating mutations, the major initiating cause of cancer. We monitored, in Escherichia coli, the kinetics of replication of both strands of DNA molecules containing a single replication block in either the leading or lagging strand. Despite a block in the leading strand, lagging-strand synthesis proceeded further, implying transient uncoupling of concurrent strand synthesis. Replication through the lesion requires specialized DNA polymerases and is achieved with similar kinetics and efficiencies in both strands.     

Biogenic amines and emotion

The studies discussed here have shown a fairly consistent relationship between the effects of drugs on biogenic amines, particularly norepinephrine, and affective or behavioral states. Those drugs which cause depletion and inactivation of norepinephrine centrally produce sedation or depression, while drugs which increase or potentiate brain norepinephrine are associated with behavioral stimulation or excitement and generally have an antidepressant effect in man (Table 1). From these findings, a number of investigators have formulated the concept, designated the catecholamine hypothesis of affective disorders (6), that some, if not all, depressions may be associated with a relative deficiency of norepinephrine at functionally important adrenergic receptor sites in the brain, whereas elations may be associated with an excess of such amines. It is not possible either to confirm or to reject this hypothesis on the basis of currently available clinical data. Although there does appear to be a fairly consistent relationship between the effects of pharmacological agents on norepinephrine metabolism and on affective state, a rigorous extrapolation from pharmacological studies to pathophysiology cannot be made. Confirmation of this hypothesis must ultimately depend upon direct demonstration of the biochemical abnormality in the naturally occurring illness. It should be emphasized, however, that the demonstration of such a biochemical abnormality would not necessarily imply a genetic or constitutional, rather than an environmental or psychological, etiology of depression.Whereas specific genetic factors may be of importance in the etiology of some, and possibly all, depressions, it is equally conceivable that early experiences of the infant or child may cause enduring biochemical changes and that these may predispose some individuals to depressions in adulthood. It is not likely that changes in the metabolism of the biogenic amines alone will account for the complex phenomena of normal or pathological affect.Whereas the effects of these amines at particular sites in the brain may be of crucial importance in the regulation of affect, any comprehensive formulation of the physiology of affective state will have to include many other concomitant biochemical, physiological, and psychological factors. Although in this review of the relationship of biogenic amines to affective state relatively little has been said concerning the intricate set of environmental and psychological determinants of emotion, the importance of these factors must be stressed. The normally occurring alterations in affective state induced by environmental events is well known to all, from personal experience. The interactions between such environmental determinants of affect, various physiological factors, and the complexity of psychological determinants, including cognitive factors derived from the individual's remote and immediate past experiences, have received only limited study under adequately controlled conditions. It may be anticipated, however, that this will prove to be a particularly fruitful area for future research, for only within such a multifactorial framework may one expect to understand fully the relationship of the biogenic amines to emotional state.