Damage control for thoracic injuries

A critically injured chest trauma patient showing profound shock or cardiac arrest en route to the trauma center or in the emergency room sometimes requires emergency room thoracotomy and definitive repair. In some patients damage control must be performed because of the appearance of the deadly triad of hypothermia, acidosis, and coagulopathy. Indications for damage control are believed to be body temperature < 34 degrees C, pH < 7.2, and clinically uncontrollable bleeding. The strategy for damage control consists of three steps: step 1, rapid control of hemorrhaging and abbreviated surgery in the ER or OR; step 2, correction of hypothermia, acidosis, and coagulopathy and reevaluation of the injuries in the intensive care unit; and step 3, definitive surgery in the OR. Damage control procedures for chest injuries include aortic cross-clamping, hilar clamping, major vessel ligation, pulmonary tractotomy, simultaneously stapled pneumonectomy or lobectomy, cardiac stapling, balloon catheter tamponade, temporary intraluminal shunt, towel packing, towel clip closure, single en masse closure of the chest wall, etc. Every surgeon responsible for treating critical chest trauma patients should have knowledge of damage control and also be familiar with the techniques.     

New Predictor for the Defecatory Function after Sphincter-Preserving Operation: Lumen Score

Few studies on sphincter-preserving surgery have analyzed the colon used for the anastomotic segment. We evaluated the usefulness of measuring the square of the diameter of the sigmoid colon (cm(2)) (lumen score, LS) as a predictor of defecatory function after very low anterior resection (VLAR) for rectal cancer. Measurements were done by radiography with semiliquid barium, and the LS was calculated. A total of 24 patients [straight coloanal reconstruction (VLAR-S), n = 17; colonic J pouch reconstruction (LVAR-J), n = 7] were studied more than 6 months after the operation. VLAR-S was divided by the LS results: the high-LS group had an LS of 12 or more (n = 5), and the low-LS group had an LS of less than 12 (n = 12). The neorectal capacity, anal manometry, and defecatory function were studied. In the VLAR-S group, LS had a significant positive correlation with neorectal capacity (gamma = 0.81, p <0.01) and a negative correlation with bowel frequency (gamma = -0.67, p <0.05). Regarding neorectal capacity, the high-LS group had a significantly larger capacity than the low-LS group (118.0 vs. 88.3 ml; p <0.05). The low-LS group had unfavorable defecatory function compared with that of the high-LS group, which was equal to that of the VLAR-J group. We concluded that the LS is a useful predictor of successful colonic J pouch reconstruction.     

Feline host range of canine parvovirus: recent emergence of new antigenic types in cats

Since the emergence of Canine parvovirus (CPV-2) in the late 1970s, CPV-2 has evolved consecutively new antigenic types, CPV-2a and 2b. Although CPV-2 did not have a feline host range, CPV-2a and 2b appear to have gained the ability to replicate in cats. Recent investigations demonstrate the prevalence of CPV-2a and 2b infection in a wide range of cat populations. We illustrate the pathogenic potential of CPV in cats and assess the risk caused by CPV variants.     

A clinical evaluation of uveitis-associated secondary glaucoma

PURPOSE: To investigate the clinical features of secondary glaucoma associated with uveitis.METHODS: The subjects of the study were 1,099 patients with uveitis (1,604 eyes) treated at the Miyata Eye Hospital, Miyakonojo, Miyazaki, between October 1974 and January 2000. The intraocular pressure (IOP) and clinical data were analyzed retrospectively. Secondary glaucoma was diagnosed in the patients when IOP was higher than 21 mm Hg at two consecutive visits and they needed treatment with medication to control the high IOP.RESULTS: Secondary glaucoma was found in 293 eyes (18.3%) of 217 patients (19.7%) among the uveitis patients. The clinical entity with the highest incidence of secondary glaucoma was Posner-Schlossman syndrome in 100%, followed by sarcoidosis in 34.1%, herpetic anterior uveitis in 30.4%, Beh?et's disease in 20.8%, human leukocyte antigen-B27-related acute anterior uveitis in 20.0%, Vogt-Koyanagi-Harada's disease in 16.4%, and human T-lymphotropic virus type 1 uveitis in 16.2%. Among these 293 eyes with secondary glaucoma, the majority (72%) had active anterior uveitis at the time of high IOP. Only 7.5% of the secondary glaucoma eyes had peripheral anterior synechia wider than 180 degrees of the trabecular meshwork. Steroid-induced glaucoma was found in only 8.9% of the secondary glaucoma eyes. Surgical therapy, mainly trabeculectomy with anti-metabolites, was performed in 38 eyes and the post-surgical IOP was controlled under 20 mm Hg in 34 eyes. Despite the medical and surgical therapy for secondary glaucoma, visual field defect was found in 39% of the secondary glaucoma eyes.CONCLUSIONS: The incidence of secondary glaucoma in the 1,604 eyes with uveitis was 18.3%, but it differed depending upon the clinical entity of the uveitis. The evaluation and the management of IOP are very important in the treatment of patients with uveitis, in addition to the management of intraocular inflammation.     

Visual evoked potentials elicited by pseudorandom stimulation from patients with macular degeneration

PURPOSE: To investigate the effect of a central scotoma on the amplitude, implicit time (IT), and temporal frequency characteristics (TFC) of the visual evoked potentials (VEPs) elicited by a pseudorandom binary sequence (PRBS) stimulus in age-related macular degeneration (AMD) patients. METHODS: Twenty-six patients with AMD, 17 eyes with visual acuity of less than 20/100, and 9 eyes with visual acuity between 20/70 and 20/25, were examined. Nine eyes of age-matched healthy volunteers served as controls. To elicit the PRBS-VEPs, one eye was stimulated with a PRBS stimulus. The first-order kernel was calculated from a cross-correlation between the PRBS and the VEPs. The Fourier transformed first-order kernel was used as the TFC of the visual system. RESULTS: The mean IT of P2 (second positive peak) of the first-order kernel was significantly delayed (t-test, P <.05), and the P2-N2 (peak-to-peak of P2 and second negative peak N2) amplitude was significantly reduced (t-test, P <.01) in eyes with AMD. A depression of the TFC values in the 6-18 Hz band was prominent in patients with AMD (t-test, P <.01). CONCLUSION: PRBS-VEPs demonstrated a prolonged IT and reduced amplitude of the first-order kernel, and reduced TFC with a reduction of visual acuity in patients with macular degeneration.     

Ciclosporin microemulsion preconcentrate treatment of patients with Beh?et's disease.

PURPOSE: The new microemulsion preconcentrate (MEPC) formulation of ciclosporin has been developed to reduce problems in intestinal absorption and to stabilize fluctuations in blood levels. A multicenter, open-label clinical trial of MEPC was conducted to assess its efficacy and safety in Beh?et's disease patients with ocular involvement. METHODS: The patient population comprised 17 de novo patients (patients not previously treated with ciclosporin in the currently available formulation) and 30 patients whose ciclosporin formulation was switched from the conventional formulation to MEPC. The patients were treated with the test formulation for 16 weeks in the former (de novo) group and for 12 weeks in the latter (switched) group. RESULTS: In the de novo group, ocular attacks decreased significantly as compared to the pretreatment incidence in 11 of the 14 patients (78.6%) evaluated after MEPC therapy. Ocular attacks also decreased significantly in the switched group. In the de novo group, visual acuity improved with MEPC therapy in 20 of the 28 eyes (71.4%) examined, and the overall efficacy evaluation was "improved" or "markedly improved" in 13 of the 16 patients evaluated (81.3%). The one case each of onset of neuro-Beh?et's disease and intestinal Beh?et's disease observed in the de novo group were regarded as adverse reactions. CONCLUSION: It was concluded that ciclosporin MEPC is useful for controlling the ocular symptoms of Beh?et's disease, and that it can be used as effectively and safely as the conventional formulation.     

Calcium influx triggers the sequential proteolysis of extracellular and cytoplasmic domains of E-cadherin, leading to loss of beta-catenin from cell-cell contacts

Cadherins are major cell-cell adhesion molecules in both tumor and normal tissues. Although serum levels of soluble E-cadherin have been shown to be higher in the cancer patients than in healthy volunteers, the detail mechanism regulating release of soluble E-cadherin remains to be elucidated. Here we show that the ectodomain of E-cadherin is proteolytically cleaved from some cancer cells by a membrane-bound metalloprotease to yield soluble form, and the residual membrane-tethered cleavage product is subsequently degraded by intracellular proteolytic pathway. Futhermore, we show that extracellular calcium influx, that is induced by mechanical scraping of cells or ionomycin treatment, enhances the metalloprotease-mediated E-cadherin cleavage and the subsequent degradation of the cytoplasmic domain. Immunocytochemical analysis demonstrates that the sequential proteolysis of E-cadherin triggered by the calcium influx results in translocation of beta-catenin from the cell-cell contacts to cytoplasm. Our data suggest that calcium influx-induced proteolysis of E-cadherin not only disrupts the cell-cell adhesion but also activates beta-catenin-mediated intracellular signaling pathway, potentially leading to alterations in motility and proliferation activity of cells.     

Significant role of neuronal non-N-type calcium channels in the sympathetic neurogenic contraction of rat mesenteric artery

1. The possible involvement of pre-junctional non-N-type Ca2+ channels in noradrenaline (NA)-mediated neurogenic contraction by electrical field stimulation (EFS) was examined pharmacomechanically in the isolated rat mesenteric artery. 2. EFS-generated contraction of endothelium-denuded mesenteric artery was frequency-dependent (2 - 32 Hz) and was abolished by tetrodotoxin (TTX, 1 microM), guanethidine (5 microM) or prazosin (100 nM), indicating that NA released from sympathetic nerve endings mediates the contractile response. 3. NA-mediated neurogenic contractions to lower frequency stimulations (2 - 8 Hz) were almost abolished by an N-type Ca2+ channel blocker, omega-conotoxin-GVIA (1 microM) whereas the responses to higher frequency stimulations (12 - 32 Hz) were less sensitive to omega-conotoxin-GVIA. The omega-conotoxin-GVIA-resistant component of the contractile response to 32 Hz stimulation was inhibited partly (10 - 20%) by omega-agatoxin-IVA (10 - 100 nM; concentrations which are relatively selective for P-type channels) and to a greater extent by omega-agatoxin-IVA (1 microM) and omega-conotoxin-MVIIC (3 microM), both of which block Q-type channels at the concentrations used. 4. omega-Agatoxin-IVA (10 - 100 nM) alone inhibited 32 Hz EFS-induced contraction by 10 approximately 20% whereas omega-conotoxin-MVIIC (3 microM) alone inhibited the response by approximately 60%. 5. These omega-toxin treatments did not affect the contractions evoked by exogenously applied NA. 6. These findings show that P- and Q-type as well as N-type Ca2+ channels are involved in the sympathetic neurogenic vascular contraction, and suggest the significant role of non-N-type Ca2+ channels in NA release from adrenergic nerve endings when higher frequency stimulations are applied to the nerve.     

Homozygous deletion of the p16/MTS-1/CDKN2 gene in malignant gliomas is infrequent among Japanese patients.

We have analyzed the status of the p16/MST-1/CDKN2 gene in 63 brain tumors from Japanese patients. With quantitative multiplex polymerase chain reaction (PCR) assay using the exon 2 primers of the p16 gene and control chromosome 9qSTS primers, we found homozygous deletion of the p16 gene in 7 cases; in 1 out of 10 cases of anaplastic astrocytomas (WHO grade III), 6 out of 35 cases of glioblastoma multiformes (grade IV) but in none of the tumors of grade I or II. We also found mobility-shifted PCR products in 8 cases using the single-strand conformation polymorphism technique. DNA sequencing of the aberrantly migrated products revealed that 5 cases of glioblastoma multiforme had mutations which caused amino acid substitutions. We found one case with silent mutations and two cases with nucleotide changes in the non-coding region. The frequency of the alteration of the p16 gene, either homozygous deletion or mutation accompanied with amino acid substitutions, increased in malignant brain tumors (grade III and IV) compared with that in low grade tumors (grade I and II) (p=0.0275), suggesting possible role(s) of the gene in the progression of brain tumors. In addition, the low frequency of homozygous deletions shown in this study is quite different from previous reports that demonstrated frequently deleted p16 gene in malignant gliomas from Caucasian patients. We have also shown the presence of heterogeneous cell populations within the glioblastoma masses based on the variety of the mutated p16 sequences. The present study, therefore, suggests a possible racial difference in the mechanism of the tumorigenesis and a heterogeneity of malignant gliomas developed during the tumor progression.