Do signs of abdominal wall injury on computed tomography predict intra-abdominal injury in trauma patients with a seatbelt sign?

BACKGROUND: A seatbelt sign in patients with blunt abdominal injury is associated with both abdominal wall and intra-abdominal injuries. This study aimed to assess the association between signs of abdominal wall injury on computed tomography (CT) and rates of intra-abdominal injury in patients with a blunt abdominal injury and a clinical seatbelt sign. METHODS: This study includes hemodynamically stable trauma patients with blunt abdominal injury and a clinical seatbelt sign who were hospitalized in two regional trauma centers in Israel, during 2014-2019. All data were collected via the medical center's trauma registry in both centers. RESULTS: We identified 123 stable blunt abdominal trauma patients with a seatbelt sign, of which 101 (82.1%) and 22 (17.9%) had a low-grade and high-grade abdominal wall injury according to CT findings, respectively. Laparotomy rates were significantly higher in patients with signs of high-grade abdominal wall injury (p<0.0001). No differences in the timing of laparotomy between low and high-grade injuries were found. CONCLUSIONS: In stable patients with blunt abdominal trauma and a clinical seatbelt sign, the severity of abdominal wall injury, as represented by CT findings, may predict a need for surgical treatment.

[Treatment of open leg fractures by double frame external fixation]. / Traitement des fractures ouvertes de jambe par le fixateur externe en double cadre

The authors review 36 cases of compound fractures of the tibia of type II and III (Cauchoix Classification). The treatment used was: 1. Careful cleansing of the sound. 2. The use of an external fixation (Hoffmann) as a double frame. 3. Continous irrigation. The authors stress that initial reduction should be accurate and that stability can be obtained by compression. Additional treatment was often needed, dependent on the stage of skin healing and the state of bone union. For the skin, Davis grafts or cross-leg flaps were used. For bone union, tibio-fibular grafts or reinforcing cancellous bone grafts (Papineau's technique) were used.

A survey on the effect of steroid hormone on type C virus production from cultured murine cells.

Dexamethasone stimulates type C virus production induced by iododeoxyuridine (IdUrd) from several murine cell lines: uninfected BALB cells, virally transformed nonproducer K-BALB cells, mouse neuroblastoma N-4 cells, and rat tumor XC cells. Dexamethasone also stimulates virus production from BALB cells newly infected by some murine leukemia or leukemia sarcoma viruses, from a murine myelogenous leukemic cell line (M-1) producing type C virus, from K-BALB(l) cells (K-BALB producing cells previously induced by IdUrd), and from K-BALB cells rescued by Rauscher leukemia virus. However, this stimulatory effect is not universal, since we observed that dexamethasone did not stimulate virus production from BALB cells newly infected by B-tropic virus, from S2CL3 cells producing N-tropic virus (a clone of spontaneously transformed BALB cells), from virus producing normal rat kidney cells, and from a mouse adrenal gland tumor Y-1 cell line chronically producing type C virus. Some estrogenic hormones that do not have any stimulatory effect on virus production from BALB or K-BALB cells induced by IdUrd stimulate virus production from normal rat kidney cells induced by IdUrd. When there is no stimulation of virus production in a cell system by steroid hormones, very often there is some inhibitory activity. Furthermore, we observed that in JLSV10 cells chronically producing Rauscher leukemia virus and in K-BALB cells newly infected by Rauscher leukemia virus, virus production is enhanced by dexamethasone when the cells are still producing a low titer of virus but is not enhanced when the cells are producing a high titer of virus.

Mechanism of stimulation of murine type-C RNA tumor virus production by glucocorticoids: post-transcriptional effects.

We have previously shown that dexamethasone stimulates production of type-C virus from seemingly normal murine fibroblasts (BALB/3T3) and from transformed (Kirsten sarcoma-leukemia virus) nonproducing cells (BALB/K3T3) induced by 5-iododeoxyuridine. In this report, we further examine the mechanism of this effect by using BALB/K3T3 cells. Several observations suggest that this effect is post-transcriptional. The optimal stimulation by dexamethasone is obtained when dexamethasone is given 24 to 48 h after 5-iododeoxyuridine induction. Although this effect is late, time course experiments suggest that dexamethasone does not act to promote release of preformed virions. The stimulation by dexamethasone is blocked when cells are treated with cordycepin (3'-deoxyadenosine) during the first 24 h of induction, but not when cordycepin is added later. Conversely, interferon, which inhibits virus production, interferes with dexamethasone when it is added late or after removal of the steroid. The results of molecular hybridization experiments show that there is no detectable increase in Kirsten sarcoma-leukemia virus-specific RNA in dexamethasone-treated cells (with or without 5-iododeoxyuridine). The results of the time course studies, and the cordycepin, interferon, and hybridization experiments, suggest that the effect of dexamethasone on type-C virus production in this system is post-transcriptional.

Adrenal corticosteroids enhance production of type-C virus induced by 5-iodo-2'-deoxyuridine from cultured mouse fibroblasts.

Induction of RNA "tumor" viruses by 5-iodo-2'-deoxyuridine in mouse fibroblasts is stimulated 5- to 25-fold by glucogenic adrenal corticosteroids. Enhancement of virus production by the hormones is inhibited by low concentration of cordycepin, an inhibitor of poly(A) synthesis.

Cordycepin inhibits induction of murine leukovirus production by 5-iodo-2'-deoxyuridine.

Cordycepin (3'-deoxyadenosine), an inhibitor of poly(A) synthesis during the processing of nuclear heterogenous RNA, blocks the production of RNA viruses induced by 5-iodo-2'-deoxyuridine in BALB/3T3 and BALB/K-3T3 cells. This inhibitory activity is not a result of either nonspecific cell killing or general cytotoxicity by cordycepin; rather, it appears to be specific, because cordycepin acts only at a critical time to inhibit virus production. These findings, together with the finding of poly(A) sequences in viral RNAs, suggest that RNA tumor viruses replicate via a transcription of proviral DNA.

In vitro induction of granulocyte differentiation in hematopoietic cells from leukemic and non-leukemic patients.

Human spleen-conditioned medium can induce the formation in vitro of large granulocyte colonies from normal human bone marrow cells. The granulocyte colonies contained cells in various stages of differentiation, from myeloblasts to mature neutrophile granulocytes. Human spleen-conditioned medium also induced colony formation with rodent bone-marrow cells, whereas rodent spleen-conditioned medium induced colony formation with rodent bone marrow but not with human cells. This in vitro system has been used to determine the potentialities for cell differentiation in bone-marrow and peripheral blood cells from patients with a block in granulocyte differentiation in vivo. The cloning efficiency, colony size, and number of mature granulocytes in bone-marrow colonies from patients with congential neutropenia, whose bone marrow contained only 1% mature granulocytes, were not less than in people whose bone marrow had the normal level of about 40% mature granulocytes. The cloning efficiency of peripheral blood cells from patients with acute myeloid leukemia was 350 times higher, with 10 times larger colonies, than the cloning efficiency of peripheral blood cells from normal people. The cytochemical properties and number of mature granulocytes in colonies from the leukemic patients were the same as in colonies from non-leukemic people. The results indicate that a block in cell differentiation in vivo, in these cases with neutropenia and acute myeloid leukemia, was overcome in vitro, in the presence of an inducer in the conditioned medium. In patients with chronic myeloid leukemia, colony formation was induced only in some of the cases. This indicates that there are blast cells with different potentialities for the development of colonies in different patients.

Feedback inhibition of the development of macrophage and granulocyte colonies. II. Inhibition by granulocytes.

It has been shown that mature normal rat granulocytes produce a substance that inhibits the activity of the inducer required for the development of macrophages (M) and granulocyte (G) colonies from normal hematopoietic cells seeded in soft agar. The granulocyte inhibitor inhibited the activity of the inducer when tested with normal hematopoietic cells from embryonic or adult organs. The inhibitor was not dialyzable, and was obtained in an active form in granulocyte-conditioned medium. The results indicate that the control mechanism that regulates the growth and development of normal macrophages and granulocytes includes a feedback inhibition of the activity of the inducer by inhibitors produced by mature granulocytes and macrophages, presumably at the end of their differentiation process. The inhibition of both M and G colonies by the feedback inhibitors produced by macrophages and granulocytes suggests that both types of colonies may be derived from a common stem cell. A line of primitive myeloid leukemia did not inhibit the activity of the inducer, and the cells of this line were not inhibited by the feedback inhibitors produced by normal granulocytes and macrophages.