Closed-chest cardiopulmonary bypass and cardioplegia: basis for less invasive cardiac surgery

BACKGROUND: We developed a method of closed-chest cardiopulmonary bypass to arrest and protect the heart with cardioplegic solution. This method was used in 54 dogs and the results were retrospectively analyzed. METHODS: Bypass cannulas were placed in the right femoral vessels. A balloon occlusion catheter was passed via the left femoral artery and positioned in the ascending aorta. A pulmonary artery vent was placed via the jugular vein. In 17 of the dogs retrograde cardioplegia was provided with a percutaneous coronary sinus catheter. RESULTS: Cardiopulmonary bypass time was 111 +/- 27 minutes (mean +/- standard deviation) and cardiac arrest time was 66 +/- 21 minutes. Preoperative cardiac outputs were 2.9 +/- 0.70 L/min and postoperative outputs were 2.9 +/- 0.65 L/min (p = not significant). Twenty-one-French and 23F femoral arterial cannulas that allowed coaxial placement of the ascending aortic balloon catheter were tested in 3 male calves. Line pressures were higher, but not clinically limiting, with the balloon catheter placed coaxially. CONCLUSIONS: Adequate cardiopulmonary bypass and cardioplegia can be achieved in the dog without opening the chest, facilitating less invasive cardiac operations. A human clinical trial is in progress.     

Streptococcus pneumoniae-induced hemolytic uremic syndrome: a case for early diagnosis

The Mitek Mini GII anchor is showcased as a relatively new device that provides a rapid, simple method for bony reattachment; here, it is introduced for the fixation of flexor or extensor tendons at their insertion. Transosseous tunnels with limited visualization, pull-out sutures, and external devices can now be avoided if desired. Applications for soft-tissue fixation should in no way be limited to the small bones of the hand. Expense of the apparatus remains its only major drawback.     

Gait pattern in the early recovery period after stroke

The gait patterns of eighteen patients who had had a single infarct due to obstruction of the middle cerebral artery were evaluated within one week after the patients had resumed independent walking and before a gait rehabilitation program had been initiated. Gait was analyzed with use of motion analysis, force-plate recordings, and dynamic surface electromyographic studies of the muscles of the lower extremities. The patterns of motion of the lower extremity on the hemiplegic side had a stronger association with the clinical severity of muscle weakness than with the degree of spasticity, balance control, or phasic muscle activity. There was a delay in the initiation of flexion of the hip during the pre-swing phase, and flexion of the hip and knee as well as dorsiflexion of the ankle progressed only slightly during the swing phase. During the stance phase, there was decreased extension of the hip that was related to decreased muscle effort and a coupling between flexion of the knee and dorsiflexion of the ankle. The abnormal patterns of motion altered the velocity, the length of the stride, the cadence, and all phases of the gait cycle. The duration of the pre-swing phase was prolonged for the patients who had the slowest gait velocities. There also were abnormal movements of the upper extremity, the trunk, the pelvis, and the lower extremity on the unaffected side in an effort to compensate for the decreased velocity on the hemiplegic side. As velocity improved, these abnormal movements decreased. Therefore, the goal of therapy should be to improve muscle strength and coordination on the hemiplegic side, especially during the pre-swing phase.     

Esophagectomy for carcinoma in the octogenarian

To correlate the findings on MRI with histopathology of metastatic melanoma, MRI was performed on 29 patients with 36 lesions, using spin-echo and inversion recovery sequences. Histopathologic examination of lesions was performed within 4 weeks of imaging. Lesions were categorized according to cell type and were also evaluated for the presence and extent of melanin, iron, and necrosis. These data were then correlated with the signal intensities of the lesions. Enhancement of lesions after injection of intravenous gadolinium was calculated and correlated to vascularity of the tumor. Melanin was present more frequently in lesions appearing hyperintense or with mixed signal intensity (12/15) than in those appearing hypo- or isointense (6/21) on the T1-weighted sequence. This trend was significant (P = .013). Also, more lesions appearing mixed, ie, having both hypo- and hyperintense components, contained melanin (15/23), as opposed to lesions that appeared to be only hyperintense (3/13) on the STIR sequence. There was no clear association between signal intensity and melanin content on the T2-weighted sequence. There was no significant association between the signal intensities on the MR images and the iron content, tumor size, or tumor cell type of these lesions. There was no clear association between enhancement after gadolinium injection and vascularity, as assessed by histology. The authors concluded in this study that T1 shortening and hypointensity on the STIR sequence seen in patients with metastatic melanoma are most closely related to the melanin content of the tumor.     

Cloning of human Stat5B. Reconstitution of interleukin-2-induced Stat5A and Stat5B DNA binding activity in COS-7 cells

We have isolated a second human Stat5 cDNA, Stat5B, and demonstrated that the genes encoding both Stat5A and Stat5B are located at chromosome 17q11.2. Both genes were constitutively transcribed in peripheral blood lymphocytes. By using specific antisera, we demonstrated that both Stat5A and Stat5B are activated by interleukin-2 (IL-2) in peripheral blood lymphocytes, natural killer-like YT leukemia cells, and human T cell lymphotropic virus type I-transformed MT-2 T cells. In COS-7 cells, which constitutively express the Janus family tyrosine kinase Jak1, reconstitution of IL-2-induced Stat5A and Stat5B DNA binding activities was dependent on the coexpression of Jak3 along with the IL-2 receptor beta chain and the common cytokine receptor gamma-chain. This IL-2-induced Stat5 activation was dependent on the presence of either of two tyrosines (Tyr-392 or Tyr-510) in the IL-2 receptor beta chain, indicating that either of these two tyrosines can serve as a docking site. Moreover, we demonstrated that human Stat5 activation is also dependent on Tyr-694 in Stat5A and Tyr-699 in Stat5B, indicating that these tyrosines are required for dimerization. The COS-7 reconstitution system described herein provides a valuable assay for further elucidation of the IL-2-activated JAK-STAT pathway.     

Neuroimmunodegeneration: do neurons and T cells use common pathways for cell death?

In syndromes of pediatric neuroimmunodegeneration (NID), certain neurons and T cells degenerate and disappear during early development at an accelerated rate without alerting the peripheral immune cells. Current studies of some of these NID syndromes suggest that the primary cause of neuronal and T cell death is an imbalanced cytokine signaling system with a dysfunctional redox status, and that the loss of T cells and neurons may be secondary to impaired functions of their accessory supportive cells. These dysfunctions include inappropriate production of developmental cytokines, inadequate secretion of reductants, and disregulation of excitotoxic amino acid metabolism. Two examples of pediatric NID in humans are ataxia telangiectasia and pediatric human immunodeficiency virus infection. An animal model is retrovirus-induced T and neuronal cell loss in neonatal mice infected with a neuroimmunopathogenic mutant, ts1, of the Moloney murine leukemia virus. Because both thymic and neuronal components share many growth factors and developmental signals, it is likely that disregulation of these signals would lead to concomitant dysfunction of neuronal and thymic cells. In this review, we focus on the pathogenic mechanisms involved in these developmental NID syndromes with the objective of identifying common pathogenic factors and pathways responsible for the concurrent losses of both neurons and T cells.