Brucellosis of unknown origin with haemophagocytic syndrome: A case report.

BACKGROUND: Brucellosis is a contagious bacterial disease caused by Brucella species, which is a leading zoonotic disease worldwide. Most patients with brucellosis have a clear infection source; however, our case had a rare presentation of secondary haemophagocytic lymphohistiocytosis without any epidemiological history. CASE SUMMARY: A 50-year-old man was admitted to our hospital with a fever of unknown origin. After laboratory examinations, such as blood culture and bone marrow biopsy, the patient was diagnosed with brucellosis and secondary haemophagocytic lymphohistiocytosis. After antibiotic therapy, the patient was afebrile, and his haemogram recovered to normal, after which he was discharged. CONCLUSION: Brucellosis cannot be excluded in patients with clinically unexplained fever, even in those without epidemiologic history.

In anemia zinc is recruited from bone and plasma to produce new red blood cells.

Anemia is highly prevalent in people with chronic kidney disease (CKD), and CKD patients always have lower plasma but higher erythrocyte Zn levels than healthy people. To date, no satisfactory mechanism has explained these Zn metabolism abnormalities. We collected blood samples from patients on hemodialysis, 5/6 nephrectomized rats and phenylhydrazine (PHZ)-induced anemic mice and rats and compared them with their normal counterparts. We found that all the anemic animals had significantly decreased plasma Zn levels but elevated erythrocyte Zn levels. We also found that in anemic mice, new red blood cells (reticulocytes) had a ~7-fold higher Zn concentration than mature erythrocytes. When excess Zn was supplied to the rats, there was a ~1.2-fold increase in the Zn level in the rat bones. When Zn was depleted in the rats, the bones lost the greatest amount of Zn in the body (a 45% decrease). We prepared Zn-depleted rats and rendered these rats anemic by treating them with PHZ, and we compared them with normal rats. We found that in PHZ-induced anemia, rats released ~16% of Zn from their bones. Rat bones not only act as a 'reservoir' to adjust the excess or deficient Zn levels but also release Zn in anemia, and the released Zn stimulates erythropoiesis in the bone marrow. In anemia, Zn is redistributed from the plasma (causing the plasma Zn level to decreases) and bones to the bone marrow to produce reticulocytes (causing erythrocyte Zn level elevation).

Apoptotic mechanisms in rabbits with blast-induced acute lung injury 1.

PURPOSE: To investigate the apoptotic mechanisms in rabbits with blast-induced acute lung injury (ALI). METHODS: A total of 40 rabbits were randomly divided into a blank control group (A, n=10) and an experimental group (EXP, n=30). Explosion-induced chest-ALI models were prepared and sampled at different time points (4, 12, and 24h after modeling, T1-T3) to test the lung dry weight/wet weight ratio (W/D) and arterial oxygen pressure (PaO2), apoptosis of lung tissue by the TUNEL assay, and Caspase-3, Bax, and Bcl-2 levels by immunohistochemical analysis. Furthermore, lung tissue was sampled to observe pathological morphology by microscopy. RESULTS: Under a light microscope, Group EXP exhibited obvious edema in the pulmonary interstitial substance and alveoli, a large number of red blood cells, inflammatory cells, and serous exudation in the alveolar cavity, as well as thickening of the pulmonary interstitial fluid. Compared to Group A, the W/D ratio was significantly increased in Group EXP (P<0.01), while PaO2 was significantly reduced (P<0.01). The apoptosis index was significantly increased (P<0.01), and caspase-3 and Bax/Bcl-2 levels were increased (P<0.01). CONCLUSION: Apoptosis plays an important role in the occurrence and development of acute lung injury in rabbits by participating in lung injury and promoting the progression of ALI.

Apoptotic mechanisms in rabbits with blast-induced acute lung injury

Abstract Purpose: To investigate the apoptotic mechanisms in rabbits with blast-induced acute lung injury (ALI). Methods: A total of 40 rabbits were randomly divided into a blank control group (A, n=10) and an experimental group (EXP, n=30). Explosion-induced chest-ALI models were prepared and sampled at different time points (4, 12, and 24h after modeling, T1-T3) to test the lung dry weight/wet weight ratio (W/D) and arterial oxygen pressure (PaO2), apoptosis of lung tissue by the TUNEL assay, and Caspase-3, Bax, and Bcl-2 levels by immunohistochemical analysis. Furthermore, lung tissue was sampled to observe pathological morphology by microscopy. Results: Under a light microscope, Group EXP exhibited obvious edema in the pulmonary interstitial substance and alveoli, a large number of red blood cells, inflammatory cells, and serous exudation in the alveolar cavity, as well as thickening of the pulmonary interstitial fluid. Compared to Group A, the W/D ratio was significantly increased in Group EXP (P<0.01), while PaO2 was significantly reduced (P<0.01). The apoptosis index was significantly increased (P<0.01), and caspase-3 and Bax/Bcl-2 levels were increased (P<0.01). Conclusion: Apoptosis plays an important role in the occurrence and development of acute lung injury in rabbits by participating in lung injury and promoting the progression of ALI.