Solid Arrow Research Articles

Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography

The assessment of left ventricular (LV) diastolic function should be an integral part of a routine examination, particularly in patients presenting with dyspnea or heart failure. About half of patients with new diagnoses of heart failure have normal or near normal global ejection fractions (EFs). These patients are diagnosed with “diastolic heart failure” or “heart failure with preserved EF.”1 The assessment of LV diastolic function and filling pressures is of paramount clinical importance to distinguish this syndrome from other diseases such as pulmonary disease resulting in dyspnea, to assess prognosis, and to identify underlying cardiac disease and its best treatment. LV filling pressures as measured invasively include mean pulmonary wedge pressure or mean left atrial (LA) pressure (both in the absence of mitral stenosis), LV end-diastolic pressure (LVEDP; the pressure at the onset of the QRS complex or after A-wave pressure), and pre-A LV diastolic pressure (Figure 1).Although these pressures are different in absolute terms, they are closely related, and they change in a predictable progression with myocardial disease, such that LVEDP increases prior to the rise in mean LA pressure. Figure 1 The 4 phases of diastole are marked in relation to high-fidelity pressure recordings from the left atrium (LA) and left ventricle (LV) in anesthetized dogs. The first pressure crossover corresponds to the end of isovolumic relaxation and mitral valve opening. In the first phase, left atrial pressure exceeds left ventricular pressure, accelerating mitral flow. Peak mitral E roughly corresponds to the second crossover. Thereafter, left ventricular pressure exceeds left atrial pressure, decelerating mitral flow. These two phases correspond to rapid filling. This is followed by slow filling, with almost no pressure differences. During atrial contraction, left atrial pressure again exceeds left ventricular pressure. The solid arrow points to left ventricular minimal pressure, the dotted arrow to left ventricular …

Anomalous Brachial Plexus Anatomy in the Supraclavicular Region Detected by Ultrasound

To the Editor: Increasingly, ultrasound is being used to assist performance of regional anesthesia. We report a previously undescribed anomaly of the superior trunk of the brachial plexus detected during performance of an ultrasound-guided supraclavicular block. A 57-yr-old man presented for elective tenolysis and reconstruction of the left hand following a previous crush injury with open fractures several months earlier. After a discussion with the patient, we chose to provide anesthesia with an ultrasound-guided supraclavicular brachial plexus block. Upon scanning the brachial plexus in the left supraclavicular fossa, we discovered that at the level of the first rib, the superior trunk was medial to the subclavian artery whereas the middle and inferior trunk was in the usual location lateral to the subclavian artery (Fig. 1). A more comprehensive scan revealed an anomalous course of the C5/C6 roots and superior trunk of the brachial plexus. The C5 root was located just lateral to the internal jugular vein, and medial to the anterior scalene muscle (ASM); the C6 root lay slightly more lateral, but still inferomedial to the ASM (Fig. 2). The C5/C6 roots remained medial to the ASM as they descended distally and coalesced into the superior trunk (Fig. 3). A similar anatomic pattern was seen on the right side.Figure 1.: Brachial plexus in the left supraclavicular region. The plexus is divided into 2 portions (arrows), one on either side of the subclavian artery (SA). The medial portion (solid arrow) was identified as the superior trunk by electrostimulation, which elicited deltoid and biceps contractions. MED = medial, LAT = lateral.Figure 2.: Brachial plexus (arrows) in the left interscalene region. The C5 and C6 nerve roots (dark circles) are clearly visible medial to the anterior scalene muscle (ASM). MED = medial, LAT = lateral, IJV = internal jugular vein, ICA = internal carotid artery.Figure 3.: Brachial plexus in the left root of the neck. The superior trunk (C5/6 nerve roots) (solid arrows) is medial to the anterior scalene muscle (ASM). The lower trunks (outlined arrow) are in their usual location in the interscalene groove. MED = medial, LAT = lateral, MSM = medial scalene muscle.We performed a supraclavicular block at the level of the first rib (Fig. 1) using an in plane approach as described by Chan et al.1 However, we modified this by performing two separate injections; first directing the needle in a medial-to-lateral, and then lateral-to-medial direction, to reach the superior trunk and the middle/inferior trunks respectively. Neurostimulation was used to confirm the identity of the superior trunk. A total of 25 mL of a 0.5% bupivacaine and 2% lidocaine admixture resulted in complete sensory and motor block. Anomalies of the upper nerve roots of the brachial plexus have been reported to occur with a frequency of 13% to 35% in the interscalene region.2–4 These usually involve an abnormal relationship to the ASM, with the C5 and C6 nerve roots either coursing through or anterior to the ASM, before assuming their normal position in the interscalene groove posterolateral to the subclavian artery. In this case, the superior trunk descended medial to the ASM throughout the posterior triangle of the neck, and remained medial to the subclavian artery even at the level of the first rib. We were unable to find a similar description of this anatomical anomaly at the supraclavicular level in the literature, although location of the inferior trunk inferior to the subclavian artery has been reported.5 Performance of either an interscalene block or a supraclavicular block in this patient using an anatomical surface landmark-guided technique would almost certainly have resulted in sparing of the C5 and C6 dermatomes. Ultrasound-guided brachial plexus blockade above the clavicle is relatively easy because the relevant structures are superficial and easily visualized. Given the prevalence of brachial plexus anomalies in the root of the neck, and the proximity of important neurovascular structures to each other, we recommend that all blocks above the clavicle should be guided by ultrasound whenever possible. Ki Jinn Chin, MBBS, FANZCA, FRCPC Ahtsham Niazi, MD, FCARCSI Vincent Chan, MD, FRCPC Department of Anesthesia Toronto Western Hospital University Health Network Toronto, Ontario, Canada [email protected]

Pancoast Hydatid Cyst Leading to Horner Syndrome

Fig. 1. (A) Preoperative chest X-ray showing: (1) the leftward displacement of the heart, (2) a linear shape of the left cardiac silhouette (arrow), and (3) a flattened right cardiac silhouette by erasure of its normally lower convexity (solid arrow). (B) Operative surgeon’s view after median pericardiotomy showing congenital partial absence of the left pericardium; note the inferior left lower pulmonary lobe (asterisk).

Targeted Ablation of Glucose-dependent Insulinotropic Polypeptide-producing Cells in Transgenic Mice Reduces Obesity and Insulin Resistance Induced by a High Fat Diet

The K cell is a specific sub-type of enteroendocrine cell located in the proximal small intestine that produces glucose-dependent insulinotropic polypeptide (GIP), xenin, and potentially other unknown hormones. Because GIP promotes weight gain and insulin resistance, reducing hormone release from K cells could lead to weight loss and increased insulin sensitivity. However, the consequences of coordinately reducing circulating levels of all K cell-derived hormones are unknown. To reduce the number of functioning K cells, regulatory elements from the rat GIP promoter/gene were used to express an attenuated diphtheria toxin A chain in transgenic mice. K cell number, GIP transcripts, and plasma GIP levels were profoundly reduced in the GIP/DT transgenic mice. Other enteroendocrine cell types were not ablated. Food intake, body weight, and blood glucose levels in response to insulin or intraperitoneal glucose were similar in control and GIP/DT mice fed standard chow. In contrast to single or double incretin receptor knock-out mice, the incretin response was absent in GIP/DT animals suggesting K cells produce GIP plus an additional incretin hormone. Following high fat feeding for 21-35 weeks, the incretin response was partially restored in GIP/DT mice. Transgenic versus wild-type mice demonstrated significantly reduced body weight (25%), plasma leptin levels (77%), and daily food intake (16%) plus enhanced energy expenditure (10%) and insulin sensitivity. Regardless of diet, long term glucose homeostasis was not grossly perturbed in the transgenic animals. In conclusion, studies using GIP/DT mice demonstrate an important role for K cells in the regulation of body weight and insulin sensitivity.

Peroxisome Proliferator-Activated Receptor β/δ Goes Vascular

See related article, pages 193–200 Peroxisome proliferator-activated receptor (PPAR)s are a family of 3 (PPARα, -β/δ, and -γ) nuclear receptor/ligand-activated transcription factors that work in concert as heterodimers with the retinoid X receptors.1 In recent years, there has been great scientific and clinical interest in the actions of PPARα and PPARγ because they are the molecular targets for the clinically used lipid-lowering fibrates and insulin-sensitizing thiazolidinedione classes of drugs, respectively.2 Until recently, very little has been known about the cellular roles of PPARδ, even though it is by far the most ubiquitously expressed of the PPAR receptors.1,3 The recent development of highly selective ligands and PPARβ/δ knockout and transgenic mice, however, have now implicated roles for PPARβ/δ in adipose tissue formation, metabolism, wound healing, brain development, placental function, colorectal carcinogenesis, and skeletal muscle function.4–6 PPARβ/δ ligands appear highly effective in regulating lipid metabolism, particularly in skeletal muscle,7,8 and are currently in phase II clinical trials for treatment of dyslipidemia, aimed particularly at individuals with low HDL levels. …

Occult cholecystitis presenting as PUO demonstrated on Gallium

Gallium-67 scintigraphy is commonly performed to investigate Pyrexia of Unknown Origin (PUO) due to its affinity for infection or inflammation. The dissemination of hybrid SPECT CT imaging allows improved identification and localisation of causes of PUO. A 74 year old male was referred for investigation of pyrexia of unknown origin. Gallium SPECT CT was performed and demonstrated increased Gallium uptake in the gallbladder wall with features of cholelithiasis and collection on the corresponding CT images. At operation the gallbladder revealed areas of chronic cholecystitis and xanthogranulomatous inflammation. Figure 1 Figure 1: A 74 year old male was referred for investigation of pyrexia of unknown origin. A Gallium scan was performed and a whole body planar and SPECT/CT were acquired up to 48 hours following the administration of 300 MBq of Ga-citrate. Gallium SPECT (Top Row) and SPECT/CT fused (Middle Row) images demonstrated increased Gallium uptake in the gallbladder wall (solid arrow). CT (Bottom Row)) images also revealed pericholecystic fat stranding (arrowhead) and a small collection at the interface between the gallbladder and the liver (solid arrow). Occult cholecystitis presenting as PUO demonstrated on Gallium 2 of 3 Figure 2 Figure 2: An ultrasound was performed for further evaluation. The US demonstrated a non-mobile calculus (solid arrow) in the gallbladder neck (Top image) and confirmed cholecystitis (Lower image) with a pericholecystic collection (solid arrow). The patient subsequently underwent laparotomy and cholecystectomy. A 39mm diameter gallstone and a haemorrhagic inflamed gallbladder were removed. Histologic examination revealed organising chronic cholecystitis and areas of xanthogranulomatous inflammation. There are number of causes of PUO including pyogenic infection (soft tissue abscess, pneumonitis, musculoskeletal), non-pyogenic infection (mycobacterial, viral, chronic bacterial, fungal/rickettsial), non-infective inflammation (sarcoidosis, inflammatory bowel disease, vasculitis, “collagen” disease, organ rejection), and neoplasia (haemoproliferative, renal cell carcinoma, melanoma). 1,2 There are a number of proposed mechanisms of 67 Ga uptake into pathologic sites including increased vascular permeability to 67 Ga-transferrin complex, radiotracer accumulation in expanded regional vascular and interstitial fluid spaces, and binding of the metal-protein complex to extravascular transferrin receptors. 3,4,5 Cholecystitis is a relatively common condition usually diagnosed clinically and confirmed by ancillary laboratory investigations and imaging with ultrasound and hepatobiliary scintigraphy. 6,7,8 The addition of Hybrid SPECT CT to 67 Ga scintigraphy improves the sensitivity and specificity of the modality in investigating PUO.

Amyloid β-Protein Precursor Juxtamembrane Domain Regulates Specificity of γ-Secretase-dependent Cleavages

Amyloid beta-protein (Abeta), the major component of cerebral plaques associated with Alzheimer disease, is derived from amyloid beta-protein precursor (APP) through sequential proteolytic cleavage involving beta- and gamma-secretase. The intramembrane cleavage of APP by gamma-secretase occurs at two major sites, gamma and epsilon, although the temporal and/or mechanistic relationships between these cleavages remain unknown. In our attempt to address this issue, we uncovered an important regulatory role for the APP luminal juxtamembrane domain. We demonstrated in cell-based assays that domain replacements in this region can greatly reduce secreted Abeta resulting from gamma-cleavage without affecting the epsilon-cleavage product. This Abeta reduction is likely due to impaired proteolysis at the gamma-cleavage site. Further analyses with site-directed mutagenesis identified two juxtamembrane residues, Lys-28 and Ser-26 (Abeta numbering), as the critical determinants for efficient intramembrane proteolysis at the gamma-site. Consistent with the growing evidence that epsilon-cleavage of APP precedes gamma-processing, longer Abeta species derived from the gamma-cleavage-deficient substrates were detected intracellularly. These results indicate that the luminal juxtamembrane region of APP is an important regulatory domain that modulates gamma-secretase-dependent intramembrane proteolysis, particularly in differentiating gamma- and epsilon-cleavages.

Using Pulse Oximetry Waveform Analysis to Guide Fluid Therapy: Are We There Yet?

In Response: I thank Dr. Michard (1) for his feedback and acknowledge his excellent review on this topic (2). I also agree that analysis of the photoplethysmographic (PPG) waveform requires care. In the past, there has been a tendency to view the PPG as a “poor man’s” arterial pressure waveform. In reality it is a volumetric signal that is the result of complex physiology which incorporates both arterial and venous components (3). Dr. Michard is correct with his assessment that the method of Fourier analysis I used in my paper (4) measures baseline (DC) modulation (which I believe would be a more accurate term then “systolic/peak value variation”). On the other hand, I disagree with his interpretation that such baseline modulation is the result of systolic pressure variation. The more common interpretation is that changes in the DC component are reflective of changes in venous blood volume. If this assertion is correct, one is left with the exciting possibility that modulation of the baseline gives access to information regarding the venous pool and pre-load status. As per Dr. Michard’s request, Figure 1 is a simple time domain analysis (Chart v 5.5, ADInstruments) of a PPG from a patient undergoing a hysterectomy, which resulted in a high estimated blood loss (approximately 1500 mL). This demonstrates that both types of modulation are present. The middle trace corresponding to fluctuations in the mean PPG value with ventilation and the bottom trace demonstrates simultaneous change in pulse amplitude (AC). It has been my observation that the modulation of the pulse amplitude is a late finding occurring with blood losses of greater than 500 mL and reflects pulse pressure variation.Figure 1.: Time domain analysis of a photoplethysmographic (PPG) waveform from a patient with significant blood loss due to a surgical procedure. The top waveform is the original PPG, the middle trace reflects changes in the mean of the waveform and the bottom trace demonstrates fluctuations in the pulse amplitude…adicht indicates ADInstruments Chart.Figure 2 shows the Fourier spectrum of the same patient demonstrating how these two types of modulation are expressed in frequency space. The solid arrow points out the effects of baseline (DC) modulation and hollow arrows point out the impact of amplitude (AC) modulation on the spectrum. This type of harmonic analysis can become particularly interesting when studied over time, using methods of joint time frequency analysis (5).Figure 2.: The Fourier analysis of the photoplethysmographic waveform from the same patient as Figure 1. The solid arrow corresponds to the modulation of the baseline (DC) component and the hollow arrows to the modulation of the pulse amplitude (AC). The cut off peak (at 1.8 Hz) corresponds to the pulse frequency (heart rate = 108) which dominates the spectrum.In answer to Dr. Michard’s letter titled “Using pulse oximetry waveform analysis to guide fluid therapy: are we there yet?” I would say “no, but we are close.” I believe we need: (1) equipment better geared to collecting the respiratory information contained in the PPG waveform, (2) algorithms refined to isolate and quantify the various types of modulation, and (3) verified interpretation of the physiology that creates the phenomenon. At that point, clinical studies focused on the sensitivity and specificity of this method over a wide range of clinical conditions can be undertaken to determine its ultimate utility. Kirk H. Shelley, MD, PhD Denis H. Jablonka, MD Aymen A. Awad, MD Robert G. Stout, MD Hoda Rezkanna, MD David G. Silverman, MD Department of Anesthesiology Yale University New Haven, Connecticut Department of Anesthesia Benha Faculty of Medicine Zagazig University Egypt [email protected]

Granzyme H destroys the function of critical adenoviral proteins required for viral DNA replication and granzyme B inhibition

Granzymes are key components of the immune response that play important roles in eliminating host cells infected by intracellular pathogens. Several granzymes are potent inducers of cell death. However, whether granzymes use additional mechanisms to exert their antipathogen activity remains elusive. Here, we show that in adenovirus-infected cells in which granzyme B (gzmB) and downstream apoptosis pathways are inhibited, granzyme H (gzmH), an orphan granzyme without known function, directly cleaves the adenovirus DNA-binding protein (DBP), a viral component absolutely required for viral DNA replication. We directly addressed the functional consequences of the cleavage of the DBP by gzmH through the generation of a virus that encodes a gzmH-resistant DBP. This virus demonstrated that gzmH directly induces an important decay in viral DNA replication. Interestingly, gzmH also cleaves the adenovirus 100K assembly protein, a major inhibitor of gzmB, and relieves gzmB inhibition. These results provide the first evidence that granzymes can mediate antiviral activity through direct cleavage of viral substrates, and further suggest that different granzymes have synergistic functions to outflank viral defenses that block host antiviral activities.

Colonic Bleeding and a Displaced Biliary Stent

Colonic Bleeding and a Displaced Biliary Stent

Sulfonylureas Correct Trafficking Defects of Disease-causing ATP-sensitive Potassium Channels by Binding to the Channel Complex

ATP-sensitive potassium (K(ATP)) channels mediate glucose-induced insulin secretion by coupling metabolic signals to beta-cell membrane potential and the secretory machinery. Reduced K(ATP) channel expression caused by mutations in the channel proteins: sulfonylurea receptor 1 (SUR1) and Kir6.2, results in loss of channel function as seen in congenital hyperinsulinism. Previously, we reported that sulfonylureas, oral hypoglycemic drugs widely used to treat type II diabetes, correct the endoplasmic reticulum to the plasma membrane trafficking defect caused by two SUR1 mutations, A116P and V187D. In this study, we investigated the mechanism by which sulfonylureas rescue these mutants. We found that glinides, another class of SUR-binding hypoglycemic drugs, also markedly increased surface expression of the trafficking mutants. Attenuating or abolishing the ability of mutant SUR1 to bind sulfonylureas or glinides by the following mutations: Y230A, S1238Y, or both, accordingly diminished the rescuing effects of the drugs. Interestingly, rescue of the trafficking defects requires mutant SUR1 to be co-expressed with Kir6.2, suggesting that the channel complex, rather than SUR1 alone, is the drug target. Observations that sulfonylureas also reverse trafficking defects caused by neonatal diabetes-associated Kir6.2 mutations in a way that is dependent on intact sulfonylurea binding sites in SUR1 further support this notion. Our results provide insight into the mechanistic and structural basis on which sulfonylureas rescue K(ATP) channel surface expression defects caused by channel mutations.

Detection of mixed‐field agglutination due to loss of red cell antigen in hematopoietic malignancy

Red blood cell (RBC) transfusions were requested for a 60-year-old woman with hypoplastic myelodysplastic syndrome (MDS) treated with cyclosporine to reverse progressive pancytopenia. During routine forward grouping, the patient typed as group A, but with mixed-field reactivity in the anti-A column of the gel card (Left panel, red box). Reverse typing with Al and B cells in the right-most two gel columns was consistent with blood group A. Common causes of mixed-field agglutination were excluded, including transfusion within the last 3 months and the presence of A-sub-groups. To further investigate the mixed-field result, we utilized an automated fluorescence cytometric blood typing method previously described by our group1'2 (Right panel. The density of antigen expression [PE fluorescence] increases from left to right; isotype control [iso] is purified polyclonal IgM). These studies showed that the patient's RBCs were group A, but could be separated into two distinguishable subpopulations that differed in their levels of A antigen expression (red line). Note that the population on the left (dashed arrow), with lower PE fluorescence, nonetheless does express residual A antigen as it is shifted to the right of the isotype control reaction (blue line). The population on the right (solid arrow) shows more usual levels of A antigen expression. In agreement with the typing results on the gel card, the patient's RBCs were negative for B antigen (black line). Thus, the mixed-field reaction seen on the gel card was due to the loss of A-antigen expression on a subpopulation of the patient's RBCs-a phenomenon that has been described in MDS patients. In addition to routine blood typing 1,2 , fluorescence cytometry is a powerful method for resolving complicated immunohematologic problems.

Retention of Core Catalytic Functions by a Conserved Minimal Ribonuclease E Peptide That Lacks the Domain Required for Tetramer Formation

Ribonuclease E (RNase E) is a multifunctional endoribonuclease that has been evolutionarily conserved in both Gram-positive and Gram-negative bacteria. X-ray crystallography and biochemical studies have concluded that the Escherichia coli RNase E protein functions as a homotetramer formed by Zn linkage of dimers within a region extending from amino acid residues 416 through 529 of the 116-kDa protein. Using fragments of RNase E proteins from E. coli and Haemophilus influenzae, we show here that RNase E derivatives that are as short as 395 amino acid residues and that lack the Zn-link region shown previously to be essential for tetramer formation (i.e. amino acid residues 400-415) are catalytically active enzymes that retain the 5' to 3' scanning ability and cleavage site specificity characteristic of full-length RNase E and that also confer colony forming ability on rne null mutant bacteria. Further truncation leads to loss of these properties. Our results, which identify a minimal catalytically active RNase E sequence, indicate that contrary to current models, a tetrameric quaternary structure is not required for RNase E to carry out its core enzymatic functions.

Hepatic Hereditary Hemorrhagic Telangiectasia

A 31-year-old woman underwent an exploratory laparoscopy for evaluation of chronic pelvic pain. She was found to have mild endometriosis; however, an incidental finding was that intraoperatively the liver was noted to be abnormal, with nodularity and discrete telangiectasias noted throughout the entire surface (Figure A). A triphasic computed tomography scan of the abdomen showed heterogeneous enhancement of hepatic parenchyma, premature opacification of hepatic veins (striped arrows), and dilated tortuous arterial branches (solid arrow) in the arterial phase (Figure B).

Percutaneous Treatment of a Large Vein Graft Aneurysm With Covered and Conventional Stents

A 75-year-old man presented with typical angina 13 years after coronary artery bypass grafting. Angiography demonstrated a patent internal mammary graft to the left anterior descending artery and vein graft to the obtuse marginal branch of the left circumflex artery. The large-caliber right coronary graft had a large false aneurysm in its midportion, at the site of a severe stenosis. The aneurysm …

Postraumatic Innominate Artery Pseudoaneurysm

i l a w a e o a p w 35-year-old man was the unrestrained driver in a ront-impact high-mechanism motor vehicle collision. valuation of the patient disclosed C1–2 lateral mass ractures, a LeFort III fracture, a mandibular coracoid rocess fracture, a left clavicle fracture, seven left-sided ib fractures, a grade I splenic injury, a grade IV liver aceration, and a left acetabular dislocation. Angiograhy, performed to evaluate a mediastinal hematoma (A), howed a 1-cm pseudoaneurysm of the innominate arery origin (B, solid arrow) and occlusion of the thyroervical trunk (B, dashed arrow).

Bond breaking at surfaces: Electrons or phonons?

The desorption of atoms and molecules is one of the most fundamental of all surface processes. A distinction is usually made between ‘‘thermal’’ desorption and desorption induced by energetic sources of excitation, such as incident photons or electrons, that induce electronic transitions. The paper by Trenhaile and co-workers in this issue shows the surprising result that the ‘‘thermal’’ desorption of Br from the Si(001) surface is in fact an electronic process in which the random statistical motion of phonons occasionally converges to excite an electron to an antibonding Si–Br r* state from which desorption of Br occurs [1]. Moreover, it is the entropy associated with the assembly of the phonons that is key to understanding how the desorption occurs. The results are important because they suggest that electronic transitions may have an important, but previously unrecognized, role in ‘‘thermal’’ desorption processes at surfaces. Bond breaking at surfaces, like its gas-phase counterpart, has long been understood based on two distinct mechanisms. In the ‘‘electronic’’ mechanism, some source of energy induces a transition from a bound electronic state to an unbound state; one example would be a transition from the Si–Br r state to a Si–Br r* antibonding state as illustrated in Fig. 1a. The second, ‘‘thermal’’ mechanism involves putting enough energy into a specific vibrational mode, such as an Si–Br stretching vibration, that a chemical bond literally breaks and desorption occurs; this process is illustrated in Fig. 1b. These mechanisms are usually distinct because the time scale for physical motion of an atom is quite long compared with the time needed for electrons to change their spatial distribution; this leads to the Franck–Condon approximation, which states that electronic transitions are usually not accompanied by a change in bond lengths and can usually be depicted as ‘‘vertical’’ transitions like that shown by the solid arrow in Fig. 1a.

Recent advances in the study of tomato Cf resistance genes

Recent advances in the study of tomato <i>Cf</i> resistance genes

Post-Mortem Three-Dimensional Reconstruction of the Entire Coronary Arterial Circulation Using Electron-Beam Computed Tomography

A 50-year-old man died suddenly while exercising on a treadmill at a local health club. He had no known previous cardiac history. During autopsy, a radio-opaque silicone compound was injected into the coronary arteries. The explanted heart was then imaged by electron-beam computed tomography (EBCT) using 3-mm slices. A complete 3D reconstruction was then obtained …

Pneumomediastinum and Severe Subcutaneous Emphysema

Figure 1. A 76-year-old man with chronic obstructive pulmonary disease was admitted after a car accident. The initial clinical and radiographic evaluation showed no evidence of rib fractures or other chest trauma. Several hours later, his neck and upper chest became increasingly swollen. Crepitations were detected on palpation of the swollen areas. Respiratory failure developed (respiratory rate, 36 per minute; pulse rate, 120 per minute; and blood pressure, 120/75 mm Hg). A chest x-ray film showed pneumomediastinum (open arrows) and extensive subcutaneous emphysema (solid arrow) that appeared in part as a cast of the muscles of the upper chest wall. . . .