Passive Pneumatic Stabilization Device for Assisting in Reduction of Femoral Shaft Fractures

Abstract During treatment of femoral shaft fractures, not only the actual fracture reduction but also the retention of the achieved reduction is essential. Substantial forces may apply to the bone fragments, due to multidirectional muscular contraction. Furthermore, forces from manipulation of one bone fragment may be transferred over the soft tissues onto the other fragments, thus hindering accurate fracture reduction. Once a sufficient reduction has been achieved, this position must be retained whilst definitive internal fixation is performed. Conventional methods comprise mounting patients on a traction table and applying manual distraction or employing special distraction devices, such as the AO distractor device. These approaches, however, only insufficiently stabilize both main fragments. For example, on the traction table the proximal femoral fragment can pivot around the hip joint thus complicating precise reduction. A novel pneumatic stabilization device to assist surgeons during operative procedures is described. This passive holding device “Passhold” connects to one main fragment through a minimally invasive bone interface and statically locks the fragment’s position. Thereafter, only the other main fragment is manipulated to achieve reduction. Mutual interference of the reciprocal fragment positions, due to soft-tissue force transfer during manipulation, is avoided. The authors examined the stability of the novel retention device on a test rig and proved its functionality under sterile settings using cadaver tests. It is concluded that this device largely facilitates the operative procedure in femoral shaft fractures, is sufficiently stable and ergonomically suitable for intraoperative deployment.     

Acute radiation reactions in oral and pharyngeal mucosa: tolerable levels in altered fractionation schedules.

PURPOSE:To investigate whether a predictive estimate can be obtained for a 'tolerance level' of acute oral and pharyngeal mucosal reactions in patients receiving head and neck radiotherapy, using an objective set of dose and time data. MATERIALS AND METHODS:Several dozen radiotherapy schedules for treating head and neck cancer have been reviewed, together with published estimates of whether they were tolerated or (in a number of schedules) not. Those closest to the borderline were given detailed analysis. Total doses and biologically effective doses (BED or ERD) were calculated for a range of starting times of cellular repopulation and rates of daily proliferation. Starting times of proliferation from 5 to 10 days and daily cellular doubling rates of 1-3 days were considered. The standard published form of BED with its linear overall time factor was used: BED=nd(1 + d/(alpha/beta) - Ln2(T - T(k))/alpha T(p) (see text for parameters). RESULTS: A clear progression from acceptable to intolerable mucosal reactions was found, which correlated with total biologically effective dose (BED in our published modeling), for all the head and neck cancer radiotherapy schedules available for study, when ranked into categories of 'intolerable' or 'tolerable'. A review of published mechanisms for mucosal reactions suggested that practical schedules used for treatment caused stimulated compensatory proliferation to start at about 7 days. The starting time of compensatory proliferation had little predictive value in our listing, so we chose the starting time of 7 days. Very short and very long daily doubling rates also had little reliability, so we suggest choosing a doubling time of 2.5 days as a datum. With these parameters a 'tolerance zone of uncertainty' could be identified which predicted acute-reaction acceptability or not of a schedule within a range of about 2-10 Gy in total BED. If concurrent chemoradiotherapy is used, our provisional suggestion is that this zone should be reduced by up to roughly 3-5 Gy10 in BED, with a request for further evidence. CONCLUSIONS:It is suggested that total BED should be used, as specified above. Parameters of alpha=0.35 Gy-(1), alpha/beta=10 Gy, Tk=7 days and Tp=2.5 days are suggested. The 'acute/ tolerance zone' then turns out to be 59-61 Gy10 for radiation-only treatments. Further information about the decrement caused by concurrent head-and-neck cancer chemoradiotherapy, possibly 3-5 Gy10, is required.     

Beiträge zur Stoffwechselphysiologie des Überlebenden Warmblüterherzens

Ohne ZusammenfassungDie Arbeit erscheint ausführlich im Arch. f. exp. Pathol. u. Pharmakol.     

Idiopathic hypereosinophilic syndrome with polymyositis

We have reported a case of idiopathic hypereosinophilic syndrome (HES) with polymyositis, in which there was marked eosinophilic leukocytic infiltration of the myocardium and striated skeletal muscles, particularly of the diaphragm, with foci of necrosis and areas of fibrosis. We believe this to be the first detailed report of the involvement of the diaphragm in HES.     

PgH2 analogs as potential antiplatelet derivatives.

Previous observations implicating PgH2 as a direct activator of platelets suggested that derivatives of U46619, a well-characterized TxA2 receptor agonist having structural homology with PgH2, might possess antiplatelet activity. The present work describes the synthesis of [1S-(1 alpha,2 beta,3 alpha,4 alpha)]-3-[(tetrahydropyranyloxy)methyl]- 2-[2-[(triphenylmethyl)oxy]ethyl]-5-oxabicyclo[2.2.1]heptane (14) a potentially useful intermediate for the synthesis of various epoxymethano derivatives. The latter was converted to [1S-(1 alpha,2 beta (Z),3 alpha,4 alpha)]-7-[3-[[2- [(phenylamino)carbonyl]-hydrazino]methyl]-5-oxabicylo[2.2.1]hept-2 - yl]-5-heptenoic acid (23), an epoxymethano derivative of PgH2 containing a hydrazide lower side chain as previously used in the TxA2 antagonist, SQ 29,548. The intermediate 14 was also converted to [1S-(1 alpha,2 beta (Z),3 alpha,4 alpha)]-7- [3-[(hexylamino)methyl]-5-oxabicyclo[2.2.1]hept-2-yl]-5-heptenoic acid (25) which contained a simple aza side chain as used in earlier antagonists. Derivatives 23 and 25 appeared to be specific antagonists of the human platelet TxA2 receptor as evidenced by their inhibition of U46619 (1.5 microM) induced aggregation of human platelet rich plasma (IC50 = 22 and 7 microM, respectively), while having little effect on ADP (2 microM) induced aggregation at much higher concentrations. In addition, one of these derivatives, the bicycloamine 25, was shown to compete for [3H]U46619 binding to washed human platelets with an IC50 value of 25 microM, supporting the notion that these derivatives were acting at the thromboxane receptor. However, the potency of these derivatives was less than for previously reported TxA2 antagonists, suggesting that simple linear combinations of functionality from molecules active at the human platelet thromboxane receptor will be of limited predictive value.