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J Port

Publications and source records attributed to J Port.

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Meniscal repair supplemented with exogenous fibrin clot and autogenous cultured marrow cells in the goat model.

This study was undertaken to evaluate the placement of fibrin clot and cultured autologous marrow cells in surgically created, full-thickness, meniscal lesions in the avascular zone in 32 female Spanish goats. The menisci were repaired with two vertically oriented sutures (N = 8), exogenous fibrin clot was placed into the meniscal defect before placement of the two sutures (N = 8), fibrin clot plus cultured adherent bone marrow cells were placed in the defect (N = 8), or the meniscal lesions were left unrepaired (N = 8). On gross and manual inspection, meniscal lesions showed some degree of healing in all animals except for the eight unrepaired lesions. All the experimental specimens had decreased tensile strength compared with the contralateral control medial menisci. Ultimate load to failure, energy absorbed to failure, and stiffness were less than 40% of the controls for all groups. Histologic sections demonstrated focal cellular areas consisting of giant cells and macrophages in the repair sites. Our observations failed to demonstrate a statistically significant enhancement of healing with the use of exogenous fibrin clot compared with vertically oriented sutures alone. The addition of cultured adherent autologous bone marrow-derived cells in conjunction with the fibrin clot did not enhance the meniscal healing.

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Hypoglycemia with glycerol salvage: a role in anti-neoplastic therapy?

UNLABELLED: Most tumors are obligate glucose consumers and severe glucose depletion has anti-neoplastic effects. However, an alternate energy source is necessary to support the host. Since glycerol is utilized by all hypoglycemic sensitive normal tissues but not tumors, glycerol may be an ideal alternate energy source. The effects of glycerol on tumor growth, animal survival during systemic hypoglycemia induced by 3-mercaptopicolinic acid (3-MP, a gluconeogenesis inhibitor), and effects of 3-MP on gluconeogenesis from glycerol were studied. Experiment 1-glycerol effect on tumor cell growth; and glycerokinase activity assay. Methylcholanthrene-induced (MCA) sarcoma cells were plated in either glucose free, glucose or glycerol containing medium. Cell counts and viabilities were recorded daily. Cells in glucose group had normal growth pattern and cell viability, while cell counts and viabilities in control and glycerol groups decreased markedly. F344 rats were injected with MCA-sarcoma cells in the flank. Glycerokinase activities in tumor and host liver were assayed on day 20. Activities were 12.3 +/- 2.8, 148.2 + 17.5 assayed on day 20. Activities were 12.3 +/- 2.8, 148.2 +/- 17.5 mumol/g protein/min in tumor and liver, respectively. Experiment 2-glycerol effect on animal survival during hypoglycemia induced by 3-MP. Following a 48 hour fast, 12 Fischer 344 rats were injected (ip) with 3-MP (200mg/kg) and randomized to saline or glycerol perfusion (100mg/kg/hr) groups. Four of 6 rats in the saline group died of hypoglycemia. All rats in the glycerol group survived, but blood glucose levels were increased as compared to the saline group. Experiment 3-3-MP effect on gluconeogenesis from glycerol as compared to lactate. 5 x 10(6) hepatocytes were incubated in glucose-free HBSS containing glycerol (20mM) or lactate (20mM) in the presence (0.5mM) or absence of 3-MP. Glucose production was assayed every 30 minutes for 2 hrs. Glucose production from glycerol was not significantly inhibited in the presence of 3-MP as compared to lactate. CONCLUSION: Glycerol does not support MCA-sarcoma growth and promotes animal survival during severe systemic hypoglycemia induced by 3-MP. However, glycerol also led to increased gluconeogenesis in this model. The use of hypoglycemic agents with glycerol protection of host tissues warrants further study.

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