Role of TNFR1 and TNFR2 in TNF-induced platelet consumption in mice

An injection of TNF in mice induced profound thrombocytopenia, due to an increase of platelet consumption, that was evident after 1 h and lasted for 3 days. This process was evident in mice that were genetically deficient in TNFR2 (p75) but not in mice lacking TNFR1 (p55), indicating that the process is mediated by TNFR1-bearing cells. To explore the site of action of TNF, labeled platelets from TNFR1 -/- or +/+ donors were transferred to TNFR1 -/- or +/+ recipients. TNF induced the consumption of platelets from TNFR1 -/- donors when injected into +/+ recipients, while platelets from +/+ donors were not consumed when present in TNFR1 -/- recipients; this finding indicates that TNF acts on the TNFR1 of host cells but does not act on platelets. The expression of TNFRs is consistent with this interpretation, since TNFRs were not detected on platelets by flow cytometry. In megakaryocytes, the expression of TNFR1 was detected by immunohistochemistry. These results indicate that TNF induces platelet consumption by acting not on platelets directly but on the TNFR1 of other cells, presumably increasing the release of factors with agonist activity for platelets.     

The effects of ginkgolide B (BN52021) on guinea pig vestibular nucleus neurons in vitro: importance of controlling for effects of dimethylsulphoxide (DMSO) vehicles

Electricity properties of polybutylcyanoacrylate nanoparticles (PBCA-NP) were studied by using a U-tube electrophoresis apparatus. It was proved that all the PBCA-NP is negatively charged. The surface potential of PBCA-NP is directly proportional to the concentration of stabilizer (Dextran 70) and the pH value of the medium, while it is inversely proportional to the concentration of butylcyanoacrylate and the model drug (gentamycin). The effect of ion strength on surface potential is obvious but not linear. The effect of stabilizers and surfactants used on the surface potential is evident while the effect of electrolytes is indistinct under the experimental conditions.     

Binding and degradation of lipoprotein(a) and LDL by primary cultures of human hepatocytes. Comparison with cultured human monocyte-macrophages and fibroblasts

Although lipoprotein(a) (Lp[a]) has structural similarities to low-density lipoprotein (LDL) that include the presence of apolipoprotein B100, there is some disagreement over the strength of its interaction with the LDL receptor and its cellular catabolism by the LDL receptor-mediated pathway. To clarify this subject we evaluated LDL receptor-mediated binding and degradation of Lp(a) and LDL in three human cell lines. The binding of 50 nmol/L Lp(a) at 37 degrees C to the LDL receptor of primary hepatocytes, macrophages, and fibroblasts was only 10%, 29%, and 29% of the respective value obtained with 50 nmol/L LDL. Analysis of 4 degrees C binding curves indicated that Lp(a) and LDL had equal affinities for the LDL receptor of fibroblasts, whereas maximal binding of Lp(a) was remarkably lower than that of LDL. LDL receptor-mediated degradation of 50 nmol/L Lp(a) in hepatocytes, macrophages, and fibroblasts was only 17%, 22%, and 26%, respectively, of the value obtained with 50 nmol/L LDL and varied greatly among the cells in that it was lowest in hepatocytes, an order of magnitude greater in macrophages, and two orders of magnitude greater in fibroblasts. In contrast, the nonspecific degradation rate of Lp(a) was similar to that of LDL in each of the three tested cell lines. However, the proportion of the degradation of Lp(a) that was nonspecific varied greatly, being 76%, 58%, and 33% in hepatocytes, macrophages, and fibroblasts, respectively. These studies indicate that not only is Lp(a) recognized by the LDL receptor but also that, in fibroblasts, Lp(a) and LDL have equal affinities for the LDL receptor, although Lp(a) has a much lower receptor occupancy than LDL. Additionally, they show that there are great cellular differences in the LDL receptor-mediated degradation of Lp(a). If these results can be extrapolated in vivo, where normal LDL levels are 40- to 50-fold higher than those of Lp(a), it would be unlikely that the hepatic LDL receptor is significantly involved in the degradation of Lp(a).     

Keratocyte loss after corneal deepithelialization in primates and rabbits

PURPOSE: To evaluate the response of stromal keratocytes to central corneal deepithelialization. METHODS: Rabbits and monkeys underwent unilateral mechanical deepithelialization with a blunt instrument and were killed at intervals ranging from 15 minutes to 24 hours after surgery. Two rabbits underwent unilateral deepithelialization under a fluid bath containing corneal preservation medium. Two rabbits were treated unilaterally with corneal preservation medium topically applied every 15 minutes for 16 hours after epithelial removal. Four rabbits underwent linear keratotomy immediately after deepithelialization of the cornea or on normal unoperated corneas and were killed 1 day (two animals) and 14 days (two animals) after surgery. RESULTS: Deepithelialization resulted in severe ultrastructural changes in keratocytes within 30 minutes after surgery. After 24 hours, the number of keratocytes in the anterior stroma underneath the deepithelialized area had decreased significantly in rabbits (P = .0001) and in monkeys (P = .0007) compared with controls. The wound healing was altered and delayed when the epithelium was not present after keratotomy. The use of storage media during and after deepithelialization minimized the early keratocyte changes and appeared to stimulate reepithelialization. CONCLUSIONS: Removal of corneal epithelium causes loss of superficial stromal keratocytes in rabbits and monkeys. Keratocyte death may results from osmotic changes that alter the corneal wound healing response.     

Production of monocyte chemoattractant protein 1 in tuberculosis patients

To investigate the role of monocyte chemoattractant protein 1 (MCP-1) in the immune response to Mycobacterium tuberculosis, we studied MCP-1 production in tuberculosis patients. CD14+ blood monocytes from tuberculosis patients spontaneously expressed higher levels of MCP-1 mRNA and protein than CD14+ monocytes from healthy tuberculin reactors. MCP-1 production in lymph nodes from tuberculosis patients was also markedly increased. These findings suggest that MCP-1 can contribute to the antimycobacterial inflammatory response by attracting monocytes and T lymphocytes.     

African-American caregiving for a relative with Alzheimer's disease

This study explored the meaning of caregiving to nine African-American caregivers of family members with Alzheimer's disease. Open-ended questions were used. Four major themes emerged from the study: caregiving is a traditional family value, caregiving is an act of love, social support is a mediator of the caregiver burden, and caregiving is a female role.     

What is your diagnosis? Pulmonary edema following changes in capillary permeability due to acute respiratory distress syndrome]

We investigated epidemiologically the risk factors of hepatitis E in Taiyuan. Of 385 patients with acute viral hepatitis collected, 191 (49.61%) were serologically identified to have hepatitis A, 104(27.01%) HB, 34 (8.80%) HE, 20 (5.19%) HC and 22 (5.72%) unidentified types. The male to female ratio of HE as 6.5 : 1. The median age of occurrence in the patients with HE was 38.5 years. One of three pregnant women with HE developed premature labor with fetal wastage. Case-control study was conducted in 70 patients with HE and 70 controls. The controls were selected from other subjects with no histories of hepatitis and matched by age and sex. The data were dealed with single factor analysis and conditional logistic regression analysis. The results showed that eating meals in resturants (OR 2.01, 95% CL 1.28-3.15), contacting with hepatitis case (OR 6.04, 95% CL 1.24-29.29), ingesting dirty drink (OR 2.16, 95% CL 2.05-2.26) are the major risk factors for HE.