PubMed · 9883159
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K L Becker, S Appling. Acute bronchitis.. https://pubmed.ncbi.nlm.nih.gov/9883159/
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We describe a 23-year-old male patient who presented with epigastric abdominal pain, 8 days following vaccination with inactivated hepatitis A virus (Haverix(R)). Clinical and laboratory data confirmed the diagnosis of pancreatitis. Repeat polymerase chain reaction (PCR) for hepatitis A replication was negative. A comprehensive evaluation ruled out other etiologies for pancreatitis. IgM Hepatitis A antibodies did not develop even after 3 months. Pancreatitis following Hepatitis A is a well-known complication of the viremia, but the exact mechanism is controversial. We suggest that the pancreatitis may have been a cellular immunlogical reaction to one of the antigens of hepatitis A virus vaccine, or it might have been caused by the release of mediators of anaphylaxis such as histamine and leucotriens, induced by HAV antigens, resulting in pancreatitis without development of humoral immunization.
Pressure is a crucial component of the cellular environment, and can lead to pathology if it varies beyond its normal range. The increased intra-ocular pressures in acute glaucoma are associated with the loss of neurons by apoptosis. Little is known regarding the interaction between pressure and apoptosis at the level of the cell. The model developed in this study examines the effects of elevated ambient hydrostatic pressure directly upon cultured neuronal lines. Conditions were selected to be within physiological limits: 100 mmHg over and above atmospheric pressure for a period of 2 hr, as seen clinically in acute glaucoma. This system can be used to investigate pressure relatively independently of other variables. Neuronal cell line cultures (B35 and PC12) were subjected to pressure conditions in specially designed pressure chambers. Controls were treated identically, except for the application of pressure, and positive controls were treated with a known apoptotic stimulus. Apoptosis was detected by cell morphology changes and by 2 specific apoptotic markers: TUNEL (Terminal transferase dUTP Nick-End Labeling) and Annexin V. These fluorescent markers were detected and quantified by automated Laser Scanning Cytometry. All techniques showed that increased pressure was associated with a greater level of apoptosis compared to equivalent controls. Our results suggest that pressure alone may act as a stimulus for apoptosis in neuronal cell cultures. This raises the possibility of a more direct relationship at the cellular level between pressure and neuronal loss.
BACKGROUND: Pig-to-primate cardiac xenografts undergo hyperacute rejection (HAR), in which primate IgM bind to porcine endothelial alpha-Gal molecules and activate membrane attack complex (MAC) deposition. Prolonged graft survival can be achieved by using transgenic pig donors, which express human complement regulatory proteins (hCRP) to inhibit MAC. However, these xenografts invariably fail from delayed xenograft rejection (DXR). We sought to investigate the poorly understood DXR process. MATERIALS AND METHODS: Wild-type (n = 3) and transgenic (n = 3) porcine hearts were heterotopically transplanted into baboons. Biopsies were analyzed by histology and by immunohistochemistry for porcine endothelial markers (vWF, alpha-Gal, and beta-Gal) and primate IgM and MAC deposition. RESULTS: Wild-type xenografts survived 60-80 min but succumbed to rapid IgM/MAC deposition and microvascular thrombosis. Transgenic xenografts avoided HAR but showed increasing IgM/MAC deposition before rejection on days 5, 7, and 11. Serum from baboons after transgenic xenograft rejection showed increased activity against porcine endothelial cells, and in vitro incubation of untransplanted porcine cardiac sections with sensitized baboon serum showed elevated microvascular IgM binding. Increased IgM deposition appeared specific to alpha-Gal, since it competes specifically with alpha-Gal-specific GS-4 lectin, but not with beta-Gal-specific RCA-1 lectin. Competition with GS-4 was not seen if naïve baboon serum was used. CONCLUSION: DXR may be mediated by increasing baboon IgM binding on porcine microvascular endothelial alpha-Gal molecules.