Determination of σ(e+e−→π+π−)\sigma(e^+e^-\to \pi^+ \pi^-) from radiative processes at DAΦ\PhiNE

We have measured the cross section $\sigma(e^+e^-\to\pi^+\pi^-\gamma)$ with the KLOE detector at DA$\Phi$NE, at an energy $W=M_\phi=1.02$ GeV. From the dependence of the cross section on $m(\pi^+\pi^-)=\sqrt{W^2-2WE_\gamma}$, where $E_\gamma$ is the energy of the photon radiated from the initial state, we extract $\sigma(e^+e^-\to\pi^+\pi^-)$ for the mass range $0.35<m^2(\pi^+\pi^-)<0.95$ GeV$^2$. From our result we extract the pion form factor and the hadronic contribution to the muon anomaly, $a_\mu$.Comment: Contributed paper to EPS 2003 and LP 200

The hadronic cross section measurement at KLOE

KLOE uses the radiative return to measure cross section σ(e+e-->π+π-γ) at the electron-positron collider DAΦNE. Divinding by a theoretical radiator function, we obtain the cross section σ(e+e-->π+π-γ) for the mass range 0.35π<0.95GeV2. We calculate the hadronic contribution to the muon anomaly for the given mass range: aμ=388.7+/-0.8stat+/-3.5syst+/-3.5t

The open abdomen in trauma and non-trauma patients : WSES guidelines

Damage control resuscitation may lead to postoperative intra-abdominal hypertension or abdominal compartment syndrome. These conditions may result in a vicious, self-perpetuating cycle leading to severe physiologic derangements and multiorgan failure unless interrupted by abdominal (surgical or other) decompression. Further, in some clinical situations, the abdomen cannot be closed due to the visceral edema, the inability to control the compelling source of infection or the necessity to re-explore (as a "planned second-look" laparotomy) or complete previously initiated damage control procedures or in cases of abdominal wall disruption. The open abdomen in trauma and non-trauma patients has been proposed to be effective in preventing or treating deranged physiology in patients with severe injuries or critical illness when no other perceived options exist. Its use, however, remains controversial as it is resource consuming and represents a non-anatomic situation with the potential for severe adverse effects. Its use, therefore, should only be considered in patients who would most benefit from it. Abdominal fascia-to-fascia closure should be done as soon as the patient can physiologically tolerate it. All precautions to minimize complications should be implemented.Peer reviewe

Goodbye Hartmann trial: a prospective, international, multicenter, observational study on the current use of a surgical procedure developed a century ago

Background: Literature suggests colonic resection and primary anastomosis (RPA) instead of Hartmann's procedure (HP) for the treatment of left-sided colonic emergencies. We aim to evaluate the surgical options globally used to treat patients with acute left-sided colonic emergencies and the factors that leading to the choice of treatment, comparing HP and RPA. Methods: This is a prospective, international, multicenter, observational study registered on ClinicalTrials.gov. A total 1215 patients with left-sided colonic emergencies who required surgery were included from 204 centers during the period of March 1, 2020, to May 31, 2020. with a 1-year follow-up. Results: 564 patients (43.1%) were females. The mean age was 65.9 ± 15.6&nbsp;years. HP was performed in 697 (57.3%) patients and RPA in 384 (31.6%) cases. Complicated acute diverticulitis was the most common cause of left-sided colonic emergencies (40.2%), followed by colorectal malignancy (36.6%). Severe complications (Clavien-Dindo ≥ 3b) were higher in the HP group (P &lt; 0.001). 30-day mortality was higher in HP patients (13.7%), especially in case of bowel perforation and diffused peritonitis. 1-year follow-up showed no differences on ostomy reversal rate between HP and RPA. (P = 0.127). A backward likelihood logistic regression model showed that RPA was preferred in younger patients, having low ASA score (≤ 3), in case of large bowel obstruction, absence of colonic ischemia, longer time from admission to surgery, operating early at the day working hours, by a surgeon who performed more than 50 colorectal resections. Conclusions: After 100&nbsp;years since the first Hartmann's procedure, HP remains the most common treatment for left-sided colorectal emergencies. Treatment's choice depends on patient characteristics, the time of surgery and the experience of the surgeon. RPA should be considered as the gold standard for surgery, with HP being an exception

SOS factors involved in translesion synthesis

Mutations are permanent DNA sequence changes that can be induced when replication occurs on a damaged DNA template. In Escherichia coli, the process of translesion synthesis past a lesion that hinders replication requires the induction of SOS-controlled gene products, among which are those of the umuDC operon. To study translesion synthesis in vivo, we have constructed single-stranded vectors containing single 2-acetylaminofluorene adducts located within −1 and −2 frameshift mutation hot spots formed by short repetitive sequences. These adducts strongly hinder DNA replication as only 2–5% of the molecules give rise to progeny under non-SOS-induced conditions. Induction of the SOS response lead to a 10-fold increase in survival. Adducts present within repetitive sequences trigger the formation of misaligned primer/template replication intermediates which, upon elongation, will result in the fixation of frameshift errors (mutagenic translesion synthesis). Surprisingly we find that elongation from the nonslipped intermediate depends upon functional umuDC(+) gene products, whereas elongation from the slipped intermediate is umuDC(+) independent but requires another, as yet biochemically uncharacterized, SOS function. These data are discussed in terms of the different steps involved during translesion synthesis through a replication-blocking lesion

Responses of skeletal muscle lipid metabolism in rat gastrocnemius to hypothyroidism and iodothyronine administration: a putative role for FAT/CD36.

Iodothyronines such as triiodothyronine (T-3) and 3,5-diiodothyronine (T-2) influence energy expenditure and lipid metabolism. Skeletal muscle contributes significantly to energy homeostasis, and the above iodothyronines are known to act on this tissue. However, little is known about the cellular/molecular events underlying the effects of T-3 and T-2 on skeletal muscle lipid handling. Since FAT/CD36 is involved in the utilization of free fatty acids by skeletal muscle, specifically in their import into that tissue and presumably their oxidation at the mitochondrial level, we hypothesized that related changes in lipid handling and in FAT/CD36 expression and subcellular redistribution would occur due to hypothyroidism and to T-3 or T-2 administration to hypothyroid rats. In gastrocnemius muscles isolated from hypothyroid rats, FAT/CD36 was upregulated (mRNA levels and total tissue, sarcolemmal, and mitochondrial protein levels). Administration of either T-3 or T-2 to hypothyroid rats resulted in 1) little or no change in FAT/CD36 mRNA level, 2) a decreased total FAT/CD36 protein level, and 3) further increases in FAT/CD36 protein level in sarcolemma and mitochondria. Thus, the main effect of each iodothyronine seemed to be exerted at the level of FAT/CD36 cellular distribution. The effect of further increases in FAT/CD36 protein level in sarcolemma and mitochondria was already evident at 1 h after iodothyronine administration. Each iodothyronine increased the mitochondrial fatty acid oxidation rate. However, the mechanisms underlying their rapid effects seem to differ; T-2 and T-3 each induce FAT/CD36 translocation to mitochondria, but only T-2 induces increases in carnitine palmitoyl transferase system activity and in the mitochondrial substrate oxidation rate

Opposing lesion structure model for NER-induced mutagenesis.

<p><b>A</b>: Nucleotide Excision Repair initiates repair at a given lesion via its normal dual incision step creating a 12–13 nt single-stranded gap. At rare occasions a second lesion will be located in the opposite strand within the initial incision gap or in close proximity. In the latter case the second lesion may becomes exposed within the gap following a gap enlargement step possibly triggered by the distortion induced by the second lesion at the double-stranded / single-stranded junction via exonuclease (or helicase) processing. The resulting structure will be referred to as “opposing lesion structure”. Alternatively, gap enlargement may result from the necessity to allow a RecA filament to assemble downstream from the lesion in order to activate Pol V [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1006881#pgen.1006881.ref047" target="_blank">47</a>]. The gap-filling process requires the action of Pol IV/Pol II. The mutation “m” opposite the lesion site is fixed by Pol V during the lesion bypass step. <b>B</b>: Mathematical modeling of UV-induced mutagenesis in a wild-type and <i>dinBpolB</i> strains as a function of UV dose (J/m²). The RiM line fits properly the <i>dinBpolB</i> data points •(dots) (regression coefficient R = 0.91). The wild-type data points ■ (squares) fit appropriately the theoretical curve when the region that defines the opposing lesion zone is set to 18 +/-3 nt (i.e. data points within the 15 and 21 nt range). <b>C</b>: Number of lesions “at risk” (LAR) as a function of UV dose (J/m²). The straight line and the quadratic curve represent the number of lesions, within the <i>rpoB</i> target, at risk for inducing mutations during replication (LAR-RiM) or during NER (LAR-NERiM: opposing lesion zone set to 18nt), respectively (see text). At ≈100J/m2, when the two curves cross, an equal number of mutations will result from replication and NER pathways.</p