Thirty-six cases of necrotizing lymphadenitis--including 33 cases of unknown etiology, 1 typhoid lymphadenopathy, and 2 cases of suspicious lupus lymphadenopathy--were clinico-pathologically reviewed and analyzed with immunostaining for s-100 and lysozyme. All cases histologically showed architectural effacement by paracortical lesions composed of nuclear karyorrhexis and mononuclear cell proliferation. Immunohistochemical study revealed proliferation of lysozyme-positive macrophages in the necrotizing areas and an increase in the number of s-100-positive cells in the uninvolved paracortical areas. This observation suggests that necrotizing lymphadenitis may be a common morphologic expression of a T cell-mediated hyperimmune condition induced by diverse etiologies.
Adolescent ; Adult ; Female ; Humans ; Immunohistochemistry ; Lymphadenitis/etiology/metabolism/*pathology ; Male ; Muramidase/metabolism ; Necrosis ; S100 Proteins/metabolism

Adult ; Antigens, CD20 ; metabolism ; Carcinoma ; metabolism ; pathology ; DNA Nucleotidylexotransferase ; metabolism ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Humans ; Keratins ; metabolism ; Lymphoma ; metabolism ; pathology ; Male ; Middle Aged ; Necrosis ; Seminoma ; metabolism ; pathology ; Thymoma ; metabolism ; pathology ; surgery ; Thymus Neoplasms ; metabolism ; pathology ; surgery ; Tuberculosis ; pathology

OBJECTIVETo evaluate the influence of necrotic tissue on progressive injury in deep partial thickness burn wounds.

METHODSTissue specimens were cultured both for estimation of IL-8, EGF, bFGF, PDGF-AB and histopathological examination, from the pre-operation, post-operation, and non-operation wounds from seven patients with deep partial thickness burn.

RESULTSIn seven specimens from the non-operation group, IL-8 release increased compared with those in the post-operation group (P < 0.001), while the levels of EGF, bFGF, PDGF-AB release were lower than those in the post-operation group. Histopathological examination revealed that in the non-operation group, the degree of neutrophil infiltration was enhanced, the extent of tissue necrosis enlarged, and residual skin appendages disappeared. In contrast, in the post-operation group, the degree of inflammatory response was decreased, with the formation of fresh granulation tissue and epithelialization.

CONCLUSIONThis study suggests that the presence of necrotic tissue could be the inhibitory factor in the wound healing process, as it might cause tissue progressive injury leading to the delay of wound healing. To promote wound healing, active tangential excision is recommended to remove necrotic tissue.

Adult ; Burns ; pathology ; surgery ; Humans ; Interleukin-8 ; metabolism ; Necrosis ; Skin ; pathology ; Wound Healing

Atherosclerosis ; immunology ; metabolism ; pathology ; Biomarkers ; metabolism ; C-Reactive Protein ; metabolism ; Endothelium, Vascular ; metabolism ; pathology ; physiopathology ; Inflammation ; metabolism ; pathology ; Inflammation Mediators ; metabolism ; Interleukins ; metabolism ; Metabolic Syndrome ; metabolism ; pathology ; Tumor Necrosis Factor-alpha ; metabolism

The changes of hyaline articular cartilage from rabbits after air exposure were evaluated. The knee joints were exposed to air for periods of thirty minutes to two hours. The animals were killed periodically, at three days, one week and three weeks postoperatively. After sacrifice, the cartilage was removed and prepared for study by light microscopy and electron microscopy. Exposure to room air for thirty minutes produced chondrocyte necrosis in the upper third of the cartilage, and exposure for 60 minutes or longer produced chondrocyte necrosis of the entire thickness of articular cartilage at three days after arthrotomy. But, three weeks after arthrotomy, we could not find any chondrocyte necrosis in any rabbits at varying periods of air exposure. There was no significant change in proteoglycan content between the aired and control cartilage. Clinical Relevance: Exposing cartilage to air can cause transient and reversible cartilage damage. If these changes are not reversible, the orthopedic surgeon should consider avoiding the prolonged exposure of articular cartilage to air, since complete matrix disintegration is known to occur months after chondrocyte necrosis.
*Air ; Animal ; Cartilage, Articular/metabolism/*pathology/ultrastructure ; Hyalin/*metabolism ; Microscopy, Electron ; Necrosis ; Rabbits ; Time Factors

Acute kidney injury (AKI) refers to a clinical syndrome in which renal function declines rapidly in a short period of time caused by various pathological factors. During the development of AKI, renal tubules with the functions of reabsorption and excretion are prone to cell death due to external pathological stimuli, which is an important cause of impaired renal function. In recent years, a variety of new cell death pathways have been gradually recognized. Researchers have now found that regulated cell death (RCD), such as necroptosis, pyroptosis and ferroptosis, are important regulatory mechanisms of AKI. This article will summarize the research advances of various types of RCD involved in the process of AKI, aiming to deepen the understanding of AKI and provide innovative thoughts for the clinical treatment of AKI.
Acute Kidney Injury/metabolism* ; Cell Death ; Humans ; Kidney/metabolism* ; Necroptosis ; Necrosis/pathology* ; Regulated Cell Death

OBJECTIVE: To study the expression and significance of TNF-alpha, MMP-9 and their relationship with the infiltration of eosinophil granulocyte in nasal polyps. METHOD: The expression of TNF-alpha and MMP-9 was determined in tissues of nasal polyps from 30 patients(nasal polyps group) and in inferior turbinate mucosa tissues from 10 patients(control group) by in situ hybridization and immunohistochemical technique, and the number of eosinophil granulocyte was counted in the same tissue by HE staining. Their correlations with each other were also analyzed in the tissue of nasal polyps. RESULT: The number of TNF-alpha and MMP-9 positive cells and TNF-alpha positive blood vessels in nasal polyps were more than that in control group (P < 0.05). The number of both TNF-alpha positive cells and blood vessels had positive relationships with the number of eosinophil granulocyte, but there was only positive relationship between the number of MMP-9 positive cells and eosinophil granulocyte (P < 0.05). At the same time there was a positive relationship between the number of TNF-alpha and MMP-9 positive cells (P < 0.05). CONCLUSION TNF-alpha and MMP-9 may play an important role in the pathological mechanism of nasal polyps. TNF-alpha may induce the expression of MMP-9 and promote the migration of eosinophil granulocyte.
Adult ; Case-Control Studies ; Eosinophils ; pathology ; Female ; Humans ; Male ; Matrix Metalloproteinase 9 ; metabolism ; Middle Aged ; Nasal Mucosa ; metabolism ; pathology ; Nasal Polyps ; metabolism ; pathology ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVE: To observe the changes of filamentous-actin (F-actin) during process of apoptosis and necrosis in hair cells, and investigate the early mark for hair cells pathology following noise exposure. METHOD: Twenty young SD rats were used in present study. The animals were randomly assigned into two groups, 10 animals were exposed noise and the remaining without exposure to noise served as normal control. The animals were exposed to a narrow band noise at 110 dB SPL for 8 hours. Immediately after exposure to continuous nose, the animals were exposed to 75 pairs of impulse noise at 155 dB SPL. The auditory brainstem response (ABR) thrush olds of both ears elicited by tone bursts at 5, 10 and 20 kHz were measured before, immediately and 2-week after the noise exposure. Animals were sacrificed and cochleae were quickly removed from the skull. Following fixation, whole specimens comprising the basilar membrane with Corti organ were separated from the modiolus. The organs of Corti were double stained with propidium iodide (PI), a DNA intercalating fluorescent probe used to visualize the morphologic viability of hair cell nuclei, and FITC-labeled phalloidin, a F-actin intercalating fluorescent probe used to visualize the morphologic viability of cuticular plate and the stereocilia in the hair cells. Each organ of Corti was thoroughly examined using fluorescence microscopy. RESULT: The animals of test group exhibited a significant elevation of ABR threshold shifts at all tested frequencies after noise exposure immediately and 2-week. There was no detectable F-actin change in both the corresponding cuticular plates and the stereocilia in the OHCs undergoing necrosis. OHCs with slightly increased PI fluorescence and a relatively normal nuclear morphology exhibited normal level of F-actin activity. In the OHCs with mild nuclear condensation (about 3/4 of the normal size) exhibited normal or a slight increased F-actin fluorescence staining. In the OHCs with moderate or severe nuclear condensation (about 1/2 or 1/4 of the normal size), the reduction in F-actin staining was observed. Finally, in the areas where no detectable nuclear staining was present, the reduction in F-actin staining was more severely or absent. CONCLUSION These results suggest that compare with the change of F-actin, nuclear morphology and staining is the early mark for necrotic and apoptotic hair cells pathology following noise exposure. A biphasic change in F-actin may exist during apoptosis, an initial polymerization and a subsequent depolymerization, but F-actin may be not a necessary component of the process of necrosis in the noise-damaged OHCs.
Actins ; metabolism ; Animals ; Apoptosis ; Cochlea ; metabolism ; pathology ; Hair Cells, Auditory ; metabolism ; pathology ; Hearing Loss, Noise-Induced ; metabolism ; pathology ; Necrosis ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo explore the effect of low-concentration lipopolysaccharide (LPS) pretreatment on hyperoxia-induced immature brain injury in neonatal mice and explore and the related mechanisms.

METHODSForty-eight neonatal mice on postnatal day 3 (PND3) were randomized into normal control group, LPS (0.3 mg/kg) group, hyperoxia group (hyperoxia exposure for 24 h), and hyperoxia+LPS group (hyperoxia exposure for 24 h 30 min after 0.3 mg/kg LPS treatment). At PND5, all the neonatal mice were sacrificed to examine the morphological changes of microglia in the periventricular white matter using Tomato lectin staining, measure malondialdehyde (MDA) content in the immature brain, detect mRNA expression of tumor necrosis factor-α (TNF-α) using real-time PCR, and determine caspase-3 protein expression with Western blotting.

RESULTSCompared with the control group, exposures to LPS, hyperoxia, and both all resulted in microglia activation in the periventricular white matter. The number of activated microglia, MDA content, TNF-α mRNA expression and caspase-3 protein expression in the immature brain were significantly higher in hyperoxia group than in the control group and LPS group (P<0.05). LPS pretreatment significantly enhanced hyperoxia-induced microglia activation in the immature brain (P<0.05).

CONCLUSIONHyperoxia causes immature brain injury mediated by microglia activation, and LPS pretreatment can enhance such brain injury in neonatal mice.

Animals ; Animals, Newborn ; Brain ; metabolism ; pathology ; Caspase 3 ; metabolism ; Hyperoxia ; Lipopolysaccharides ; adverse effects ; Malondialdehyde ; metabolism ; Mice ; Mice, Inbred C57BL ; Microglia ; metabolism ; pathology ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo investigate the effect of the iron chelator deferoxamine (DFA) in suppressing microglia activation and protecting against secondary neural injury in a rat model of intracerebral hemorrhage (ICH).

METHODSSD rats were randomly divided into sham-operated group, ICH group and DFA treatment group. ICH model was established by infusion of type IV collagenase into the right basal ganglia, and starting from 1 h after the operation, the rats received intraperitoneal DFA injections every 12 h for 7 days. The iron content in the perihematoma brain tissue was determined at different time points after DFA administration, and OX42 immunohistochemistry was used to observe the changes in the microglia. The contents of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the brain tissue were detected by ELISA. The neural death and neurological deficiency were measured using Nissl staining and neurological scores, respectively.

RESULTSThe iron content in the brain tissues around the hematoma was significantly increased 3 days after ICH and maintained a high level till 28 days, accompanied by a marked increase of microglial cells as compared to the sham-operated group. DFA injection caused significantly decreased iron content in the brain tissue, reduced number of microglial cells, and lowered levels of IL-1β and TNF-α. Neuronal loss around the hematoma was obviously reversed after DFA injections, which resulted in improved neurological deficiency.

CONCLUSIONDFA can suppress microglia activation by removing iron overload from the perihematoma brain tissue, thus reducing secondary neuronal death and neurological deficiency in rats with ICH.

Animals ; Cerebral Hemorrhage ; metabolism ; pathology ; Deferoxamine ; pharmacology ; Interleukin-1beta ; metabolism ; Iron ; metabolism ; Male ; Microglia ; drug effects ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; metabolism