Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 7 de 7
Filter
Add filters








Type of study
Year range
1.
Journal of Forensic Medicine ; (6): 586-595, 2023.
Article in English | WPRIM | ID: wpr-1009391

ABSTRACT

The coronavirus disease 2019 (COVID-19) has been a global epidemic for more than three years, causing more than 6.9 million deaths. COVID-19 has the clinical characteristics of strong infectivity and long incubation period, and can cause multi-system damage, mainly lung damage, clinical symptoms of acute respiratory distress syndrome (ARDS) and systemic multiple organ damage. The SARS-CoV-2 virus is still constantly mutating. At present, there is no global consensus on the pathological changes of COVID-19 associated deaths and even no consensus on the criteria for determining the cause of death. The investigation of the basic pathological changes and progression of the disease is helpful to guide the clinical treatment and the development of therapeutic drugs. This paper reviews the autopsy reports and related literature published worldwide from February 2020 to June 2023, with a clear number of autopsy cases and corresponding pathological changes of vital organs as the inclusion criteria. A total of 1 111 autopsy cases from 65 papers in 18 countries are included. Pathological manifestations and causes of death are classified and statistically analyzed, common pathological changes of COVID-19 are summarized, and analytical conclusions are drawn, suggesting that COVID-19 infection can cause life-threatening pathological changes in vital organs. On the basis of different health levels of infected groups, the direct cause of death is mainly severe lung damage and secondary systemic multiple organ failure.


Subject(s)
Humans , SARS-CoV-2 , COVID-19/pathology , Cause of Death , Lung/pathology , Autopsy
2.
Journal of Clinical Surgery ; (12)1999.
Article in Chinese | WPRIM | ID: wpr-552214

ABSTRACT

Objective To analyze the patients with the portal hypertension.Methods We analyzed 121 cases with gallbladder pathologic changes from 391 cases with portal hypertension.Results Among 391 cases,52.1% were posthepatitic type, 24.8% were composites type,4.1% were ethanol type,4.1% were bile type,11.5% were bilharziasis type,1.7% were latent type,1.7% were peculiar type;81 cases were proved with gallbladder wall thicker and rougher, double shadow or cholecysitis,14 cases were proved cholestatis sludge,51 cases with gallbladder stones or single stone,5 cases with gallbladder polyps,5 cases with gallbladder wither, 7 cases with choledocholiths.Conclusion Portal hypertention,insufficient hepatic function, ascites and hypersplenism are the main causes of cholecystis pathologic changes in patients with portal hypertension.

3.
Korean Journal of Orthodontics ; : 297-310, 1998.
Article in Korean | WPRIM | ID: wpr-656085

ABSTRACT

The purpose of this study was to investigate the initial tissue change, to repair on the teeth & surrounding tissue under the intrusive orthodontic forces by use of elastic chain, through the microscopic findings. For this-study, three young adult mongrel dogs were used, and were divied into three group ; the control group was deliveried only casting crown, and the experimental group I was equipped with energy chain during I week, and experimental 2 group was deliveried using energy chain during 1 week, and 3 weeks observation. All experimental groups and control groups were sacrificed to make the samples for microscopic findings on premolar teeth. All samples were examed and compared the histologic changes through the microscopic with H-E stain. The obtained results were as follows. 1. In hematoxylin-eosin stain of the control group, the periodontal ligament was constant width from apical third to cervical third of the root, and the periodontal fiber arrangement was horizontal or oblique in cervical third, oblique in middle and apical third of the root. 2. In Masson Trichrome stain of the control group, osteoblast and osteoclast appeared in cervical third of root , and bone resorption and new bone formation was observed in middle and apical third of the root. 3. In experimental 1, osteoclasts were increased highly, and hyperemia of blood vessels and new bone formation and bone resorption by reversal line in apical third of the root were seen. PDL width was increased apprarently from crest to apex of the root and more in apical third. 4. In experimental 2, osteoclasts and hyperemia of blood vessels were more increased than control material in apical third of the root. PDL width was increased more than control group in root apex, and was seen less than experimental 1. PDL arrangement was similar to experimental i and was mixed only in root apex. Therefore, in premolar intrusion of the young adult dog, there were increased osteoclast, hyperemia and dilation of blood vessel, resorption of alveolar bone and cementum, and different arrangement of PDL in initial tissue change. There was not observed complete repair after remove intrusive force.


Subject(s)
Animals , Dogs , Humans , Young Adult , Bicuspid , Blood Vessels , Bone Resorption , Crowns , Dental Cementum , Hyperemia , Osteoblasts , Osteoclasts , Osteogenesis , Periodontal Ligament , Tooth
4.
Journal of Korean Neurosurgical Society ; : 1441-1445, 1997.
Article in Korean | WPRIM | ID: wpr-91291

ABSTRACT

The effects of radiosurgery on the arteriovenous malformation(AVM) nidus are documented in some studies as endothelial hypertrophy followed by obliteration of the vascular lumen with thrombosis. According to the literature total angiographic obliteration of the AVM nidus after radiosurgery takes about two years, but few reports of the histologic changes after radiosurgery for AVM are found. The authors encountered a case in which AVM surgery was performed after three months of LINAC radiosurgery because of the AVM bleeding. Histologic changes seen in the AVM nidus after three months of radiosurgery were the endothelial hypertrophy and the perivascular inflammation as early features of obliteration.


Subject(s)
Hemorrhage , Hypertrophy , Inflammation , Radiosurgery , Thrombosis
5.
Ciênc. rural ; 25(2): 233-238, 1995. ilus, tab
Article in English | LILACS | ID: lil-529704

ABSTRACT

Trypanosoma evansi caused severe anemia in horses and pronounced leukopenia in dogs, both naturally infected. The horses presented microcytic normochromic anemia and the dogs showed microcytic hypochromic anemia. The clinical signs observed were fever, anemia, edema of the legs and lower parts, weakness and inappetence. Light microscopic studies demonstrated that Trypanosoma evansi produced several alterations in erythrocytes of dogs and horses. These pathologic changes included vacuolation, acanthocytes, dacrocytes, codocytes, microspherocytes and bizarre shapes. Mature erythrocyte were observed adhered to trypanosomes. Erythrophagocytosis was also demonstred.


Trypanosoma evansi produziu severa anemia em cavalos e pronunciada leucopenia em cães, ambos naturalmente infectados. Os cavalos apresentaram anemia microcítica normocrômica e os cães desenvolveram uma anemia microcítica hipocrômica. Os sinais clínicos foram febre, anemia, edema das pernas e porções inferiores, fraqueza e inapetência. Estudos com microscopia ótica demonstraram que o Trypanosoma evansi produziu várias alterações nos eritrócitos dos cães e cavalos. Estas alterações patológicas incluíram vacuolação, acantócitos, dacrócitos, codócitos, microesferócitos e formas bizarras. Eritrócitos maduros foram observados aderidos a tripanosomas. Eritrofagocitose foi também observada.

6.
Chinese Pharmacological Bulletin ; (12)1987.
Article in Chinese | WPRIM | ID: wpr-551482

ABSTRACT

Ketoconazole(KET) is a new imi-dazole derivative with broad antimycotic spectrum. In order to verify the clinical toxic and side effect and its properties in animals, we made a long-term toxicity test for 30 days. Dosages of 70, 35 and 17. 5 mg?kg-1?d-1(e-quivalent to 21, 10. 5 and 5. 2 times of the clinical dosage) were given ig to dogs. The salivation , vomiting, anorexia, decrease in heart rate and loss of weight occurred in the large dosage group. Half of the dogs died from toxicosis within ig 15 days. Laboratory examination showed that the activities of ALT, LDH and ALP, the content of T-BIL, BUN in serum in-creased in this group. Pathological examination revealed that there were some pathological changes in the liver, kidneys, adrenal glands and sex gland in the group. There were no significant changes in other dosage groups compared with the normal control group. After withdrawal of KET, all toxic symptoms disappeared and the abnormal indexes were restored. The results indicated that toxic target organs of KET were liver, kidney, adrenal gland and sex glands. The safe dosage for dogs was about 17. 5 mg?kg-1?d-1.

7.
Academic Journal of Second Military Medical University ; (12)1982.
Article in Chinese | WPRIM | ID: wpr-549758

ABSTRACT

Preclinical toxicology of PsD-007(a new photosensitizer prepared in our coll-ege)was studied.Pathological observations were performed on major organs of the toxic dogs including liver, kidneys, myocardium, lungs, spleen, stomach, intestine, mesenteric lymph nodes, urinary bladder, prostata, testes, ovary, adrenals, pituitary gland, thyroid and brain.Focal balloning degeneration of hepatic cells occurred in lower dose groups, and degeneration and necrosis of hepatocytes and proximal convoluted tubular epithelial cells of kidney, and edema of brain in higher dose groups were observed in acute toxicity testing.The hepatocytes were normal, but hyperplasia, swelling and vacuoles within the cytoplasm of the Kupffers cells in liver, necrosis of tubules of kidney and edema of brain in higher dose groups were found in subacute testing. These damages were reversible within 4 weeks except in higher dose groups, and their morphologic severity was dose-related.The results show that the liver and kidney may be the main target organs of toxicity of PsD, and the detections of hepatic and renal functions may be useful to guard against its toxic effects during clinical use.

SELECTION OF CITATIONS
SEARCH DETAIL