The article summed up the experience of CHEN Ying-yi in treating chronic diarrhea.Chen held that the main pathogenesis of chronic diarrhea were the disharmony between the liver and the spleen,commonly impairing the function of kidney,therefore the treatment principle should focus on regulating the liver and invigorating the spleen. Invigorating the spleen should distinguish replenishing qi,tonigying yin and warming yang.Regulating the liver had to discriminate the excess and defi ciency of liver's conveyance and dispersion.Long-time diarrhea will impair the function of kidney.If it damaged the kidney-yang,we should warm up Governor Vessel to lift the kidney-yang.If it damaged the kidney-yin,we should nourish kidney-yin by replenishing kidney-yang.In this article,the author listed the basic prescription of CHEN Ying-yi in treating chronic diarrhea and his clinical experience,which can be used as references in clinic practice.

Objective: To investigate the effects of carotid arteriosclerosis on cognitive functions and current prognosis in patients with cerebral infarction. Methods: Extracranial carotid arteries were assessed using dopple ultrasongraphy in 112 patients with cerebral infarction. Cognitive functions were evaluated with the Mini-Mental state Examination (MMSE) and five neuropsychological tests assessing memory, attention, calculation psychomotor rapidity and visuospatial perception. Deficits in neurological functions were assessed on admission and 3 to 4 weeks. Results:All neuropsychological measures were found to be poorer in patients with carotid arteriosclerosis than those with no carotid arteriosclerosis, especially in cases with severe carotid arteriosclerosis and severe carotid stenosis. There was a positive relationship between severity of carotid arteriosclerosis and change in cognitive functions. The scores of SSS were higher on admission in cerebral infarction patients with carotid arteriosclerosis. Recent prognosis was also poorer in patients with carotid arteriosclerosis.Conclusions: Significant effect of carotid arteriosclerosis was shown on cognitive functions of patients with cerebral infarction. As cerebral ischemic injury is severe, prognosis in cerebral infarction patients with carotid arteriosclerosis is poor.

Objective To study the clinical significance of carotid atherosclerosis and the relationship between carotid atherosclerosis and cerebral infarction recurrence.Methods Carotid atherosclerosis was assessed using doppler ultrasongraphy in 312 patients with cerebral infarction, the duration of following up was 12 to 18 months,and the characteristics of carotid atherosclersis was compared to patients with or without recurrence cerebral infarction.Results Of the 312 patients with cerebral infarction, 61 patients suffered from new cerebral infarction during following up period, the recurrence rate in patients with atherothrombotic brain infarction was higher than those with lacunar infarction, and the cerebral infarction recurrence usually occurred in the same side of initial stroke of the 57 patients with severe carotid atherosclerosis, 26 patients had a sufference of new infarction, of the 48 patients with high grade stenosis, 25 had a sufference of new cerebral infarction, of the 42 patients with ulcerated plaque, 23 had sufference of new cerebral infarction,showing a recurrence rate significantly higher than those patients with non carotid atherosclerosis or those with mild carotid atherosclerosis. The logistic regression analysis showed that the levels of carotid atheroslerosis , stenosis and ulcerated plaque were positively related to the cerebral infarction recurrence.Conclusions There is a positively relationship between carotid atherosclerosis and cerebral infarction recuurrence, and the level of carotid atherosclerosis is a risk factor of cerebral infarction recurrence.It serves as a risk marker of cerebral infarction recurrence.

Objective To investigate the expression of cyclooxygenase-2 (COX-2) and epidermal growth factor receptor (EGFR) in astrecytomas, as well as the correlation between them. Methods The expression of COX-2, EGFR and PCNA were respectively detected by immunohistochmical (S-P) method in 68 astrocytomas and 5 cases normal brain tissue. Proliferation index (PI) was calculated and the correlation of COX-2, EGFR and PI was analyzed. Results COX-2 and EGFR were negative expression in normal brain tissue. The positive expression rate of COX-2 and EGFR in high grade astrocytomas was significantly higher than that in low grade astrocytomas(73.53% vs 44. 18% ,67.65% vs 38.24%, P <0. 01 ), and the PI was significantly higher than that in low grade astrocytumas as well as normal brain tissue(46.11 ± 10. 68vs 23. 04±6. 25,4. 52±0. 95, P <0. 01 ). The PI in COX-2 positive group was higher than that in negative group( P <0. 01 ). The positive expression rate of COX-2 in the group with EGFR positive expression was higher than that in the negative group. Conclusions The expression of COX-2 and EGFR was related to pathological feature of astrocytomas. COX-2 may promote the proliferation of tumor cells. There was a static correlation between the expression of EGFR and COX-2 in astrocytomas. EGFR signal transduction probably modulated the expression of COX-2 in astrocytomas cells.

Objective:To investigate the pathological characteristics and the clinical significance of novel coronavirus (2019-nCoV)-infected pneumonia (termed by WHO as coronavirus disease 2019, COVID-19).Methods:Minimally invasive autopsies from lung, heart, kidney, spleen, bone marrow, liver, pancreas, stomach, intestine, thyroid and skin were performed on three patients died of novel coronavirus pneumonia in Chongqing, China. Hematoxylin and eosin staining (HE), transmission electron microcopy, and histochemical staining were performed to investigate the pathological changes of indicated organs or tissues. Immunohistochemical staining was conducted to evaluate the infiltration of immune cells as well as the expression of 2019-nCoV proteins. Real time PCR was carried out to detect the RNA of 2019-nCoV.Results:Various damages were observed in the alveolar structure, with minor serous exudation and fibrin exudation. Hyaline membrane formation was observed in some alveoli. The infiltrated immune cells in alveoli were majorly macrophages and monocytes. Moderate multinucleated giant cells, minimal lymphocytes, eosinophils and neutrophils were also observed. Most of infiltrated lymphocytes were CD4-positive T cells. Significant proliferation of type Ⅱ alveolar epithelia and focal desquamation of alveolar epithelia were also indicated. The blood vessels of alveolar septum were congested, edematous and widened, with modest infiltration of monocytes and lymphocytes. Hyaline thrombi were found in a minority of microvessels. Focal hemorrhage in lung tissue, organization of exudates in some alveolar cavities, and pulmonary interstitial fibrosis were observed. Part of the bronchial epithelia were exfoliated. Coronavirus particles in bronchial mucosal epithelia and type Ⅱ alveolar epithelia were observed under electron microscope. Immunohistochemical staining showed that part of the alveolar epithelia and macrophages were positive for 2019-nCoV antigen. Real time PCR analyses identified positive signals for 2019-nCoV nucleic acid. Decreased numbers of lymphocyte, cell degeneration and necrosis were observed in spleen. Furthermore, degeneration and necrosis of parenchymal cells, formation of hyaline thrombus in small vessels, and pathological changes of chronic diseases were observed in other organs and tissues, while no evidence of coronavirus infection was observed in these organs.Conclusions:The lungs from novel coronavirus pneumonia patients manifest significant pathological lesions, including the alveolar exudative inflammation and interstitial inflammation, alveolar epithelium proliferation and hyaline membrane formation. While the 2019-nCoV is mainly distributed in lung, the infection also involves in the damages of heart, vessels, liver, kidney and other organs. Further studies are warranted to investigate the mechanism underlying pathological changes of this disease.