Theoretical calculations of the reaction cross-sections for proton-induced reactions on natural copper using ALICE-IPPE code

A theoretical study of the nuclear-reaction cross sections for proton-induced reactions on (63)Cu and (65)Cu was performed in the proton energy range from threshold values up to 50MeV. The produced nuclei were different isotopes of Zn, Cu, Ni, Co and Mn, some of which have important applications. The reaction cross-section calculations were performed using the ALICE-IPPE code, which depends on the pre-equilibrium compound nucleus model. This code is suitable for the studied energy and isotopic mass ranges. Approximately 14 excitation functions for the different reactions have been constructed from the calculated cross-section values. The excitation function curves for the proton reactions with natural copper targets have been constructed from those for enriched targets using the natural abundance of the copper isotopes. Comparisons between the calculated excitation functions with those previously experimentally measured are given whenever the experimental values were available. Some statistical parameters were introduced to control the quality of the fitting between both the experimental and the theoretical calculated cross-section values.     

Acupuncture therapy for sleep-related laryngospasm

Sleep-related laryngospasm is a rare disorder that may cause severe disablement. It refers to episodic arousal from sleep with a sense of suffocation followed by stridor. This phenomenon, which is caused by laryngospasm, is probably secondary to gastroesophageal reflux. The reflux is the target for current treatment of this serious disorder. Treatment by acupuncture for sleep-related laryngospasm has not been previously reported in the English medical literature. We describe a previously healthy patient with sleep-related laryngospasm caused by gastroesophageal reflux refractory to current medical treatment who was treated successfully using acupuncture.     

Relationship between the paraoxonase 1 gene glutamine 192 to arginine polymorphism and gestational diabetes mellitus in Saudi women

Objectives

Gestational diabetes mellitus (GDM) is recognized as an imbalance between insulin resistance and insulin secretion, leading to maternal hyperglycemia. Previous studies in a Saudi population indicated a high frequency of Paraoxonase 1 glutamine 192 to arginine (PON1 Q192R) polymorphism, suggesting this polymorphism as an additional risk factor. The present study was designed to explore the possible association between the PON1 Q192R polymorphism and GDM in a Saudi population.

Methods

This case–control study was carried out in 500 pregnant women, including 200 GDM cases and 300 non-GDM women. Genotyping for PON1 Q192R (rs662) variants was performed by polymerase chain reaction–restriction fragment length polymorphism (PCR–RFLP).

Results

The results of the present study indicates that Q192R polymorphism was significantly associated with GDM in a Saudi population with the minor allele frequency (MAF) (p = 0.0007). Q192R genotypes and alleles showed a strong association with GDM (p = 0.009 and p = 0.0007, respectively).

Conclusion

In conclusion, these findings suggest that the PON1 Q192R polymorphism has high MAF in GDM in the studied Saudi population.     

Alterations of platelet function and clot formation kinetics after in vitro exposure to anti‐A and ‐B

BACKGROUND: ABO‐mismatched platelets (PLTs) are commonly transfused despite reported complications. We hypothesized that because PLTs possess A and B antigens on their surface, ABO‐mismatched transfused or recipient PLTs could become activated and/or dysfunctional after exposure to anti‐A or ‐B in the transfused or recipient plasma. We present here in vitro modeling data on the functional effects of exposure of PLTs to ABO antibodies. STUDY DESIGN AND METHODS: PLT functions of normal PLTs of all ABO types were assessed before and after incubation with normal saline, ABO‐identical plasma samples, or O plasma samples with varying titers of anti‐A and anti‐B (anti‐A/B). Assays used for this assessment include PLT aggregation, clot kinetics, thrombin generation, PLT cytoskeletal function, and mediator release. RESULTS: Exposure of antigen‐bearing PLTs to O plasma with moderate to high titers of anti‐A/B significantly inhibits aggregation, prolongs PFA‐100 epinephrine closure time, disrupts clot formation kinetics, accelerates thrombin generation, reduces total thrombin production, alters PLT cytoskeletal function, and influences proinflammatory and prothrombotic mediator release. CONCLUSIONS: Our findings demonstrate a wide range of effects that anti‐A/B have on PLT function, clot formation, thrombin generation, PLT cytoskeletal function, and mediator release. These data provide potential explanations for clinical observations of increased red blood cell utilization in trauma and surgical patients receiving ABO‐nonidentical blood products. Impaired hemostasis caused by anti‐A/B interacting with A and B antigens on PLTs, soluble proteins, and perhaps even endothelial cells is a potential contributing factor to hemorrhage in patients receiving larger volumes of ABO‐nonidentical transfusions.     

Relationship between tumor necrosis factor‐alpha and ammonia in patients with hepatic encephalopathy due to chronic liver failure

BACKGROUND. We have recently demonstrated that in humans, circulating levels of tumor necrosis factor‐α (TNF) correlate positively with severity of hepatic encephalopathy (HE) due to chronic liver failure.

AIM. The main aim of this larger population study is to determine the relationship between TNF and ammonia in patients with HE and chronic liver failure due to liver cirrhosis.

METHODS. Circulating levels of TNF and ammonia were measured in 108 patients with liver cirrhosis due to various etiologies in various clinical grades of HE (grades 0–4). TNF concentrations were measured in venous serum using commercially available solid‐phase high sensitivity enzyme‐linked immunosorbent assay. Ammonia levels were determined in venous plasma by the enzymatic method, using the glutamate dehydrogenase reaction.

RESULTS. The mean±SEM values of circulating levels of TNF and ammonia at presentation in patients with grade 0 of HE (n = 30) were 3.89±0.2?pg/mL and 49.8±2.8?µg/mL respectively, in patients with grade 1 of HE (n = 26) were 8.56±0.34?pg/mL and 101.6±6.5?µg/mL respectively, in patients with grade 2 of HE (n = 22) were 11.59±0.48?pg/mL and 160.3±10.7?µg/mL respectively, in patients with grade 3 of HE (n = 20) were 19.98±0.94?pg/mL and 228.8±16.1?µg/mL respectively, and in patients with grade 4 of HE (n = 10) were 51.53±8.59?pg/mL and 284.2±20.3?µg/mL respectively. A significant positive correlation was found between circulating levels of TNF and those of ammonia (r = 0.62, P<0.0001), and also between circulating levels of both substances and severity of HE in these patients (r = 0.95, P<0.0001, and r = 0.9, P<0.0001 respectively). TNF and ammonia were both significant independent predictors of severity of HE (P<0.0001 for both variables).

CONCLUSION. The results of this study demonstrate a significant relationship between TNF and ammonia in patients with chronic liver failure and HE, and so strengthen the suggestion that TNF could be strongly involved in the pathogenesis of HE in these patients. Hence, we suggest a new theory in the pathogenesis of HE, the ‘TNF theory’.