The present study is an attempt to further asertain the histological location and afferent connections of the "Groaning Center" of cat.In 1952, by electrical stimulation of the lateral tegmental area of cats, a restricted region was found to give rise to the groaning response and it was designated as the "Groaning Center", which on excitation would also produce various viseral and motor reactions.According to our microscopic study of the position of the "Groaning Center", we found that the nucleus subcuneiformis in the lateral tegmental region is the focal point of the center. It lies ventralateral to the nucleus trochlear, medial to the lateral lemniscus and the nucleus paralemniscalis (Jasper atlas, 1954), dorsal to the nucleus cuneiformis. This center extends about 1.0 mm. anteroposteriorly, 1.0 mm. mediolaterally and about 1.5 mm. dorsoventrally. This area cheifly consists of fibers and scattered cells of medium and small size. A cluster of larger cells has been observed in the ventral region of the center.By HRP retrograde transport study, we found that after injection of HRP into the center, the reactive cells were found in extensive brain areas. The labelled cells were mainly found in the ipsilateral side of the hypothalamus, especially in the lateral and posterior nucleus of hypothalamus as well as the dorsomedial nucleus of hypothalamus. The reactive cells were also found in the forebrain regions, such as the cingulate gyrus, globus pallidus, zona incerta, nucleus parafa-sicularis, etc.The relation between the center with vocalization and emotional responses is discussed.

The effects of foot-shock (FS) on ir-?-EP and ir-NT in the brain and pituitary of unanaesthetized rats were studied by means of radioimmunoassay (RIA). It was found that the content of ir-?-EP decreased significantly in pituitary and increased in hypothalamus, and the content of ir-NT increased both in pituitary and hypothalamus 2 min after FS. However, ir-?-EP increased in pituitary and decreased in hypothalamus, and ir-NT decreased both in pituitary and hypothalamus 20 min after FS. These results indicate that at the early period of FS induced stress, the release of ir-?-EP may be increased from pituitary, and ir-NT may be decreased from both pituitary and hypothalamus.

Diabetic neuropathy is the most common peripheral neuropathy,and it is important to enhance both nerve regeneration and prevent nerve degeneration in its treatment. Disturbed nerve regeneration in diabetes has been ascribed,at least in part,to decreases of some neurotrophic factors or the decreases of their receptor expressions.This paper reviewed the effect of some major neurotrophic factors on diabetic neuropathy and their application in clinical treatment.

In this study, acute cardiac ischemia was induced by ligation of the anterior descending branch of the coronary artery in rats. Radioimmunoassay was conducted to measure the contents of immunoreactive beta - en-dorphin (ir-?-EP)after ischemia and fructose -1,6 - diphosphate (FDP) treatment. Results showed that the contents of ir-?-EP were in-cereased in the plasma, some brain areas, pituitary and myocardium after ligation of the left coronary artery of the rats which resulted in the deterioration of the cardiac function includingdp/dtmax, Lvsp, total areas of force loop and blood pressure. Intravenous administration of FDP improved cardiac function and reduced the contents of ir - ? - EP in the above mentioned tissues suggesting that ir-?-EP correlate closely with cardiac function after ischemia,the reduction of which was possibly involved in the improve ment of cardiac function by FDP.

Objective To investigate the effects of levocarnitine combined with urimetazidine on left ventricular remodeling in maintenance hemodialysis(MHD)patients.Methods All of 86 MHD patients and 40 healthy volunteers(health control group)were involved in the study.all of 86 MHD patients were randomly divided into two groups,disease treatment group(46 cases)and disease control group(40 cases),who had undergone hemodialysis for at least 3 months before the study and were in a stable clinical status without signs of infection or disease activity.In disease treatment group,1.0 g of levocarnitine was infused at the end of each dialysis treatment and 20 mg of trimetazidine was taken orally 3 times each day for 6 months,while the parameters for free fatty acid(FFA),free carnitine(FC),inflammation and oxidative stress were studied before and after the treatmenL In disease control group these two drugs were not used.The left ventricular end-diastolic diameter(LVDd),left ventricuhr end-systolic diameter(LVDs),left atrial diameter (LAD),left ventricular posterior wall thickness(LVPWT),interventricular septal thickness(IVST)and left ventricular ejection fraction(LVEF)were detected by ultrasonic cardiography.Results Before treatment,the serum levels of FFA,high-sensitivity C-reactive protein(hs-CRP),intedeukin(IL)-1β,IL-6,tumor necrosis factor(TNF)-αand malondialdehyde(MDA)were higher in disease treatment group and disease control group than those in health control group(P<0.05 or<0.01),while the serum levels of FC,glutathione peroxidase(GSHPx)and superoxide dismutase(SOD)were lower in disease treatment group and disease control group than those in health control group(P<0.05 or<0.01).Compared with those before treatment,the serum levels of FFA,hs-CRP,IL-1β,IL-6,TNF-α,MDA were decreased(P<0.05 or<0.01),FC,GSHPx,SOD were increased(P<0.05 or<0101),the scores of LVDd,LAD,IVST,LVPWT,LVMI were also decreased significantly(P<0.05),while LVEF increased markedly after treatmem in disease treatment group(P<0.05).There were significant differences in all indexes between disease treatment group and disease control group(P<0.05 or<0.01).Conclusion Supplements of levocarnitine combined with trimetazidine in MHD patients appear to be associated with an improvement of left ventricular remodeling.

Objective To investigate the effect of L-carnitine on pathological changes of myocardium and the underlying mechanism in chronic renal failure rats (CRF). Methods A total of 55 male SD rats were randomly divided into sham group (n=10),model group (n=15),low dose (300 mg/kg),medium dose (600 mg/kg) and high dose (900 mg/kg) L-carnitine group(n=10,each).5/6 subtotal nephrectomy was performed in these rats without sham group.One week after the operation,normal saline or corresponding dose L-carnitine were intragastrically administrated to sham and model group or L-carnitine groups for 17 weeks.Transthoracic echocardiography,mean arterial pressure (MAP),heart rate (HR) and heart weight/body weight were assessed.Moreover,24h urine protein,renal function,SOD,MDA,IL-6,ATP,ADP were measured at the end of the study.Additionally,pathological changes in myocardium were detected by light microscope and transmission electron microscope. Results (1) ATP (μmol/g·wt)in L-carnitine groups (2.35±0.24,3.59±0.28,3.78±0.25) was significantly higher than that in model group (1.61±0.12) (all P＜0.01).(2) Thickness of posterior wall of left ventricle (mm) in high dose L-carnitine group was thinner than that in model group (3.74±0.23 vs 4.18±0.48,P＜0.05). (3) The ratios of heart weight to body weight in both medium dose and high dose L-carnitine groups (3.92±0.27,3.65±0.2) were significantly lower compared to model group (3.99±0.27) (all P＜0.01). (4) Under light microscopy,disarrangement and hypertrophy of cardiac myocytes,increased myocardial fibrosis were observed in model group, while these changes and the pathological scores were significantly improved in both medium dose and high dose L-carnitine groups (7.14±1.07,6.13±0.99),as compared with model group (9.88±1.13) (all P＜0.01).Under electron microscopy,typical changes in cardiac hypertrophy were observed,including dissolution of myocardial fibers,increasing and swelling of mitochondria,membrane rupture as well as matrix increase in model group,while these changes were ameliorated by L-carnitine in a dose-dependent manner. (5) Seventeen weeks after the treatment,both IL-6 and MDA were decreased in all L-carnitine-treated groups than those in model group [IL-6 (ng/L):261.86±13.18,240.12±18.7,233.34±36.88 vs 596.64±81.41; MDA (nmol/L):15.23±2.01,12.41±0.6.10.97±1.9 vs 21.84±2.71).Whereas,SOD (U/ml) were increased in L-carnitine-treated groups (51.2±6.11,58.51±5.52,60.63±6.94) than that in model group(32.01 ±5.69 )(all P＜0.05).(6) No significant differences of systolic,diastolic blood pressure or MAP were found among groups. Conclusion L-carnitine can improve energy metabolism,micro-inflammation and oxidative stress in myocardium of CRF rats,which may be associated with the amelioration of cardiac hypertrophy and fibrosis.

Objective To study effects of recombinant ciliary neurotrophic factor(CNTF) on the changes of JAK\|STAT pathway and tyrosine phosphorylation in the injured neurons. Methods Sciatic nerve of rat was resected and sutured into silicone tube with local infusion of recombinant CNTF.The distribution and quantity of STAT3 and phosphotyrosine(PTyr) immunoreactivity in the neurons of L3\|L5 spinal anteriolateral nuclei and L5 spinal ganglion were observed and measured by immunohistochemical ABC method with computer image analysis. Results There was much STAT3 immunoreactivity in the neuron located in the nucleus of spinal anteriolateral nuclei.PTyr immunoreactivity showed higher in the cell membrane of spinal anteriolateral nuclei and in the cytoplasma and neucleus of spinal ganglion in CNTF group than that in SAL group.Conclusion\ The results suggest JAK\|STAT pathway in the injured motoneurons be activated and strengthened and tyrosine phosphorylation in the injured neurons be enhanced by recombinant CNTF.\;[

Objective To study effects of recombinant ciliary neurotrophic factor (CNTF) on gene expression of Schwann cells in the injured peripheral nerves. Methods Sciatic nerve of rat was resected and sutured into silicone tube with local infusion of recombinant CNTF.One or two weeks after nerve repaired,the distribution and quantity of S100 protein (S100),growth associated protein 43 (GAP-43), phosphotyrosine (PTyr) and signal transducer and activator of transcription 3(STAT3) immunoreactivity in the distal nerve of the injured sciatic nerve were observed and measured with immunohistochemical ABC method by computer image analysis. Results S100,GAP-43,PTyr and STAT3 immunoreactivity showed significantly higher in the distal nerve of the injured sciatic nerve in CNTF group than that in SAL group.Conclusion\ Recombinant CNTF could up-regulate the expressions of S100,GAP-43,PTyr and STAT3 in Schwann cells of the injured peripheral nerve.The results suggest that the JAK-STAT pathway can be strengthened,and the expressions of S100 and GAP-43 can be subsequently up-regulated by recombinant CNTF in Schwann cells.

The changes of immunoreactive neurotensin (ir-NT) contents in the brain areas, pituitary gland and plasma in the trautized rats were observed by radioimmunoassay. The results showed the significant changes of the ir-NT contents in the hypothalamus, pituitary gland, plasma, injured tissue, hippocampus, central gray and spinal cord in the posttraumatic rats at different intervals. A predominant characterization of the change of ir-NT levels in the brain areas, pituitary gland and plasma, was the dramatical decrease at various times except for the hypothalamus, central gray, and hippocampus with biphasic alterations. The ir-NT contents in the frontal cortex, pons and medulla also displayed changes to different extent under the acute craniocerebral trauma condition These results suggest that NT may play a role in the pathophysiology of traumatic injury.

The neuropeptide orexins, including orexin A and orexin B, are located exclusively in hypothalamus OX1R and OX2R are receptors of orexin. OX1R is selective to orexin A while OX2R is not. The distributions of orexin neurons in human brain are the same as those of rats. Orexin was closely related with sleep and awakening behavior besides regulating the feeding behavior. Orexin-containing terminals are also found in areas modulating sleep and awakening such as the locus ceruleus, tuberomammillary nucleus, dorsal raphe, and the basal forebrain. In those areas, there are also lots of OX1R and OX2R and their precursors. Orexin neurons are extremely active during rapid wave sleep and awakening. If hypothalamus in some areas is destroyed and orexin neurons are reduced, sleep-awakening dysfunction will appear (for instance: narcolepsy).