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Y P Guo

Publications and source records attributed to Y P Guo.

At least 19 recordsLinked to original sources
PubMed1998

L-propionyl carnitine, an endogenous ester in fatty acid metabolism, exerts anti-shock and endothelial protective effects in rat splanchnic ischemia-reperfusion injury.

Splanchnic artery occlusion (SAO) results in a severe form of circulatory shock in which oxygen-derived free radicals play an important role. L-Propionyl carnitine (LPC), an endogenous ester that plays a crucial role in cellular fatty acid oxidation and metabolism, has been shown to exert a protective effect in myocardial ischemia/reperfusion injury. Our purpose was to investigate the effects of LPC in an SAO model of ischemia/reperfusion injury. Pentobarbital-anesthetized rats were subjected to 60 min of SAO followed by 120 min of reperfusion. An intravenous bolus of LPC (200 microg/kg) administered 2 min before reperfusion prolonged survival time (116+/-4 vs. 81+/-3 min in 1 mL/kg .9% NaCl vehicle, p < .01), increased survival rate (88 vs. 13.6%, p < .01), and attenuated the percent increase in hematocrits (27+/4% vs. 43+/-3%, p < .05), and the increases in tissue myeloperoxidase activity (1.76+/-.4 U/100 mg vs. 3.79+/-.2 U/100 mg, p < .05). In addition, LPC increased mean arterial blood pressures at 60 min (p < .05), 80 min (p < .05), 100 min (p < .05), and 120 min (p < .05) postreperfusion. Moreover, LPC markedly attenuated splanchnic artery endothelial dysfunction induced by SAO ischemia/reperfusion injury (maximal vasorelaxation to ACh, 74+/-2.7% vs. 57+/-1.9% in vehicle, p < .01). In this murine SAO model of ischemia/reperfusion injury, LPC affords significant protection that may be achieved through inhibiting leukocyte infiltration into intestinal tissue and preserving endothelial function, thereby decreasing microvascular permeability and maintaining tissue perfusion.

Animals↗
PubMed1997

Cell proliferation and death in the irradiated pituitary gland and its modification by growth stimulants.

PURPOSE: This study was undertaken to show whether the rate of expression of radiation injury in the rat pituitary gland could be accelerated by the use of growth stimulants. METHODS AND MATERIALS: Rat pituitary glands were irradiated in situ with a range of single doses up to 20 Gy. The rats were then given subcutaneous slow-release implants containing 17beta-estradiol (E2) and sulpiride (S) to stimulate lactotroph proliferation. Two sequential cycles were used, each consisting of stimulation (3 weeks) and withdrawal (2 weeks). Measurements were made of gland weight; BrdU-labeled, giant, and apoptotic cells; lactotrophs; as well as pituitary prolactin content, in response to exogenous thyroid-releasing hormone (TRH). RESULTS: The two cycles of stimulation/withdrawal resulted in marked changes in gland weight, BrdU-labeling index, and serum prolactin (PRL) levels in unirradiated rats. The proportion of immunopositive growth-hormone-producing (GH) cells increased after irradiation. Radiation inhibited the hypertrophic response to E2 + S and also inhibited increases in BrdU-labeling index and serum PRL levels. Also, giant lactotrophs were observed in the irradiated pituitaries. However, they were not seen in the unirradiated rats or in the irradiated rats treated with E2 + S. TRH promoted PRL secretion in the unirradiated rat. In contrast, TRH inhibited PRL secretion in the irradiated rat and in all treatment groups receiving E2 + S. Apoptosis was induced by irradiation and was substantially increased in lactotrophs and in other cell types by withdrawal of the E2 and S stimulus, although the highest observed incidence was only 7 per 10,000 cells. CONCLUSION: Both irradiation and E2 + S treatment removed the hypothalamic control of PRL secretion, which reveals this important inhibitory action of TRH upon PRL secretion. This suggests that it is not suitable as a dynamic test of pituitary PRL reserves in such abnormal situations, where there may also be damage to the hypothalamic-pituitary vasculature. The increasing proportion of GH cells after irradiation indicates that lactotrophs respond more rapidly to irradiation. The stimulation by E2 + S somehow prevented the radiation-damaged lactotrophs from becoming giant cells. Also, the ratio of apoptotic cells to BrdU-labeled cells was increased by the E2 + S treatment, indicating that the E2 + S did enhance radiation-induced cell death relative to cell renewal. However, overall, the E2 + S stimulus protocol did not promote a dramatic increase in cell death (apoptosis) nor a marked decrease in residual gland weight after irradiation. Hence, its use would probably not be beneficial in the treatment of slow-responding prolactinomas, if malignant lactotrophs respond similarly to the normal pituitary lactotrophs. However, the observation of induced apoptosis after hormone and drug withdrawal suggests that agents which promote tumor shrinkage may be effective by causing rapid apoptosis of tumor cells in vivo.

Animals↗
PubMed1996

Time course of radiation-induced apoptosis in the adult rat spinal cord.

Radiation-induced apoptosis has been reported in thymic, lymphoid, haematopoietic cells and intestinal epithelium but is infrequently documented in other adult mammalian cell types. In this study, we examined the time course of radiation-induced apoptosis in the adult cervical rat spinal cord following a single dose of 8 or 22 Gy. Apoptosis was assessed by morphological criteria under light and electron microscopy, and immunohistochemically in-situ using Apoptag to detect 3' -OH ends of DNA fragments. Little evidence of apoptosis (0.3 +/- 0.1 apoptotic nuclei per spinal cord section) was observed in control un-irradiated spinal cord. A significant increase in the number of apoptotic cells per spinal cord section was seen at 4 h after 8 (13.6 +/- 1.3) or 22 Gy (22.0 +/- 2.7). The number of apoptotic nuclei reached a peak at 8 h (44.7 +/- 3.7 after 8 Gy, 49.5 +/- 4.3 after 22 Gy), and returned to the baseline level by 24 h (2.4 +/- 0.7 after 8 Gy, 3.3 +/- 0.7 after 22 Gy). A dose of 22 Gy induced significantly more apoptoses than 8 Gy at 4, 6, 10 and 12 h (P < or = 0.033), but not at 8 h. More apoptotic nuclei were observed in white matter (64-92%) than gray matter (8-36%). All the apoptotic cells were observed in glial cells, and there was no evidence of radiation-induced apoptosis in the vascular endothelial cells or neurons. The morphological features of the apoptotic cells under electron microscopy and the absence of GFAP staining suggested that they were oligodendrocytes. We conclude that radiation induces apoptosis in the adult rat spinal cord, and that the development of apoptosis follows a specific time course.

Animals↗
PubMed1994

[Effects of T4 monomer of Tripterygium wilfordii and artificial musk on experimental allergic neuritis].

UNLABELLED: Both T4 monomer of Tripterygium wilfordii and artificial musk had effects in regulating immune system and anti-inflammation. The effect of using artificial musk was the earlier the stronger. According to pharmacological features of the two drugs and pathogenesis of experimental allergic neuritis (EAN), 5 experimental groups were established, i.e., artificial musk prevented and treated groups, dexamethasone and T4 monomer treated groups, and control group. RESULTS: T4 monomer could reduce the clinical score of model rabbits of EAN and significantly ameliorated inflammatory cell infiltration and demyelination. It was similar to dexamethasone. Although artificial musk had mild preventing and treating effects on the clinical and pathological changes of EAN, but was not statistically significant in comparing with control group. Our clinical or pathological data suggested that T4 monomer and dexamethasone were effective in the treatment of EAN, and that of artificial musk in preventing and treating EAN as indefinite.

Animals↗
PubMed1992

[Hereditary motor and sensory neuropathy].

The report consisted of 10 cases of hereditary motor and sensory neuropathy (HMSN). There were 7 males and 3 females. Their ages ranged from 11 to 42 (average 24.6) years, ages of onset varied from 7 to 34 (average 17.3) years. Hereditary history was showed in 4 cases. The clinical features of all 10 cases had peroneal muscular atrophy, 8 of 10 cases also had involvement of the upper limbs, 7 of 10 cases had pes arcuatus. The conduction velocity was obviously slow in 5 cases and slightly slow in the others. Oion-bulb hypertrophic neuropathy was demonstrated in sural nerve biopsies of 5 cases. Neuronal axonal degeneration were found in the remaining 5 cases. Clinical classification, clinical features and pathological characteristics were discussed.

Adolescent↗
PubMed1992

[Mitochondrial myopathy of progressive external ophthalmoplegia].

UNLABELLED: Ten cases of blepharoptosis and chronic progressive oculomuscular paralysis are reported among which three had limb muscular weakness. Sex: male 5, female 5. Age: 16-58 years old. Age of onset: 7-38 years old. DURATION: 2-26 years. Muscle biopsy showed ragged red fibers, abnormal mitochondria and paracrystalline mitochondrial inclusions under both light and electron microscopy. All cases were diagnosed as CPED (chronic progressive external ophthalmoplegia) clinically and abnormal mitochondria pathologically.

Adolescent↗
PubMed1992

[Mitochondrial myopathy with peripheral neuropathy].

UNLABELLED: This paper reported mitochondrial myopathy with peripheral neuropathy of 2 cases. Both patients were males. Age: 22, 32. DURATION: 11, 14 years respectively. They showed recurrent paralysis and asthenia of limbs. Case 1 was motor sensory neuropathy, whose EMG revealed neurogenic injury. Case 2 involved only the lower limbs, whose lactic acid level was increased. In both patients, muscle biopsy showed Ragged Red fibers and abnormal mitochondria. Sural nerve biopsy revealed moderate reduction in the number of mylinated fibers and chronic axonal degeneration without regeneration cluster and hypertrophic neuropathy. Electron microscopic examination showed the increase of Schwann cells and mitochondria, and abnormal mitochondria being less marded in Case 2. Mitochondrial myopathy with peripheral neuropathy and its pathogenesis were discussed.

Adult↗
PubMed1991

Vasculitic neuropathy. A clinical and pathological study.

The clinical, electrophysiological and pathological features and prognosis of 34 patients with peripheral neuropathy caused by necrotizing vasculitis were evaluated. The causes included polyarteritis nodosa and its Churg-Strauss variant, rheumatoid arthritis, undifferentiated connective tissue disease, Wegener's granulomatosis, primary Sjögren's disease, and chronic lymphocytic leukaemia with cryoglobulinaemia; 2 patients had no evidence of systemic vasculitis. Mononeuritis multiplex was the most common clinical manifestation, followed by asymmetrical polyneuropathy and distal symmetrical polyneuropathy. Pain was a frequent symptom. Nerve conduction studies were abnormal in all cases, and in 3 patients there was conduction block or severe slowing of motor conduction. Necrotizing vasculitis was present in sural nerve biopsies of most cases, and severe active axonal degeneration was a dominant feature. Immunofluorescent staining of blood vessels for immunoglobulin, C3 and fibrinogen was positive in all cases in which it was performed, even when there was no cellular infiltration. All patients were treated with prednisone alone or in combination with other immunosuppressive agents, or with plasmapheresis. Long-term follow-up studies demonstrated that although the peripheral neuropathy usually improved and caused only mild to moderate functional disability, the long-term prognosis of the systemic disease was poor with a 5-yr survival of only 37%.

Adult↗
PubMed1991

[Diabetic neuropathy: a clinical and pathological study of 8 cases].

Eight cases of diabetic neuropathy are reported, including 5 cases of mixed type sensori-motor-autonomic neuropathy and 3 cases of mononeuropathy multiplex. Sural nerve examination was made in 8 cases. Pathological study showed not only demyelination of the myelinated fibres, but also axonal degeneration. There was different degree of thickening of vascular wall and stenosis of vascular lumen in these 8 cases, one of which showed thrombosis of small vessels in between the nerve fascicles. Marked thickening of basement membrane of the endothelial cells of the blood vessel and of the Schwann's cells was identified by electron-microscopy. The muscles in 5 cases showed neurogenic changes, and one of these 5 cases exhibited syndrome of diabetic amyotrophy. The pathological changes, clinicopathological classification and pathogenesis of the disease are discussed.

Aged↗
PubMed1991

[A variant form of Guillain-Barre syndrome: a study of clinical and pathology of sural nerve biopsy].

This study reported four cases of variant of Guillain-Barre Syndrome (GBS). Clinical features showed muscle fasciculation, Fisher Syndrome, GBS with family Leber's disease and idiopathic dysautonomia. There were oligoclonal protein in 3 patients and elevation of protein of CSF in 4 cases. The neurogenic lesion of limb muscle was confirmed by EMG and NCV in all patients. The sural nerve biopsy was characterized by inflammatory demyelination. The diagnosis and pathogenesis were discussed.

Adolescent↗
PubMed1991

[A clinical study of recovery of memories in 46 cases of cerebrovascular diseases].

The authors reported the application of a clinical memory scale to 46 patients with cerebrovascular diseases after administration of nimodipine or placebo by using the double-blind method of study and making careful clinical observation, evaluation and statistical treatment. It is shown that nimodipine can increase the memory quotient (MQ) of patients with cerebrovascular diseases (P less than 0.01). The relation between the patients age and cultural background, the site and nature of the lesion and the degree of memory recovery was discussed.

Aged↗
PubMed1991

[Amyotrophic lateral sclerosis: an analysis of 167 cases].

167 cases of amyotrophic lateral sclerosis treated in Peking Union Medical College Hospital were analyzed. There was a significant difference between some of the clinical features of amyotrophic lateral sclerosis in China and western countries. The age of onset in China was 10 to 20 years earlier than and the male to female ratio (4.6:1) was 2 times higher than those in the west. Average age of death was 47 years, being earlier than that in the west. Some specific clinical features for early clinical diagnosis were also discussed.

Adolescent↗
PubMed1990

Introduction of the activated N-ras oncogene into human fibroblasts by retroviral vector induces morphological transformation and tumorigenicity.

The introduction of activated N-ras cDNA into normal diploid human skin fibroblast cell cultures using the retroviral vector pZIPneo results in a spectrum of morphologies ranging from near normal to, in rare instances, dense piled-up colonies of morphologically transformed cells. However, none of the clones isolated were transformed as assessed by growth on agar or tumorigenicity in nude mice. Introduction of both c-myc and N-ras oncogene cDNAs into normal skin fibroblasts failed to produce transformation as assessed by growth on agar and tumorigenicity in nude mice, although c-myc infection alone conferred immortality and the resultant doubly infected cell line was immortal. Using the same construct, activated N-ras cDNA was shown to transform immortalized human fibroblasts to tumorigenicity. However, immortalization per se was shown not to guarantee 'co-operation' with an activated N-ras gene to give malignant transformation. Although numerical and structural chromosome aberrations (clonal and non-clonal) were observed in some of the cell strains isolated after retroviral infection, these were not directly associated with viral infection, the presence of the oncogenes or with the morphologically transformed phenotype.

Animals↗
PubMed1990

[Polymyositis associated with peripheral nerve lesion: clinico-pathological investigation of 8 cases].

UNLABELLED: Polymyositis with peripheral nerve lesion are rare. The study of eight cases of polymyositis with some peripheral lesion, pathologic investigation of muscle biopsy of all patients and biopsy of sural nerve in six cases were reported. Age: 19-52 (average 34) yrs. COURSE: 4mo-10 (average 4) yrs. They showed symmetric weakness and tenderness of the proximal muscles, peripheral hypoesthesia and hypo even areflexia. Electrophysiological parameters showed myogenic lesion in 8 cases and neurogenic in 3 cases. Pathological (light and electron-microscopic) findings coincide with acute and chronic myositis, consisting of focal necrosis of muscle fiber, monocyte infiltration, myofibril regeneration, hyperplasia of interstitial vessels and fibrous tissue in muscle biopsy of 8 cases; mild to moderate loss of density of myelinated fibers, mostly thin myelin sheath and demyelinating changes, axonal degeneration also, mainly loss of unmyelinated fiber, perivascular monocyte and macrophages in sural nerve biopsy of six cases. The aforementioned clinical and pathological findings suggest that involving both muscle and nerve be able to primary. No primary course involving nerve has been found, except in only one case with coexisting SLE, another case six months later carcinomatous myositis was diagnosed, but there are no evidence of vasculitis and ischemic neuropathy.

Adult↗
PubMed1990

[Pathological changes in the vagus nerves in chronic alcoholism].

A systematic morphometric examination of the vagus nerves at different levels obtained at autopsy in 4 control subjects and 6 alcoholic patients. Morphometric studies on myelinated fibres were performed on the nerve at the mid-cervical, lung hilum and diaphragmatic levels. In the patients with alcoholic neuropathy there was a significant reduction in density of myelinated fibers in the distal part of the vagus nerves when compared with controls. The more severe distal degeneration in the nerves and the pathological changes of axonal degeneration distally are consistent with the dying back neuropathy. The relation between the secondary segmental demyelination and degeneration of the involved nerves were discussed.

Adult↗
PubMed1989

Becker muscular dystrophy.

Five patients from 3 families with Becker muscular dystrophy (BMD) were reported. The main clinical and laboratory findings were in common. Pairs of affected brothers are quite resembled each other. However, there are also some variations among different families. The disease occurred later in the first pair of brothers and was accompanied by macroglossia and red-green color blindness, while the second pair got the disease earlier, which was accompanied by heart impairment. It is interesting that both myogenic and neurogenic changes of EMG can be found in the same patient with BMD in our series.

Adolescent↗