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1.
J Anim Sci ; 95(1): 379-386, 2017 Jan.
Article in English | MEDLINE | ID: mdl-28177366

ABSTRACT

The effects of supplementing lambs with Co, either alone or in combination with vitamin B and Se, were evaluated over the period from weaning to selection for slaughter. Two hundred and five recently weaned (at 14 wk [SD 0.44] of age), spring-born lambs of various crossbred genotypes were stratified, within genotype, by BW and gender and allocated to 3 groups, which were then allocated at random to one of the following treatments: no supplement (Control), a supplement containing Co only (Co-only), or a supplement containing Co, vitamin B, and Se (VitMin). The concentration of Co in the Co-only supplement was 2.1 mg/mL (as cobalt sulfate); the VitMin supplement contained Co (10 mg/mL, as cobalt acetate), vitamin B (200 µg/mL), and Se (0.25 mg/mL, as sodium selenite). Lambs on the Co-only and VitMin treatments received, every 14 d, 10 and 2.1 mL, respectively, of oral drench. Lambs were managed in a rotational-grazing system from 12 July (swards predominantly ) and selected for slaughter, on the basis of BW, after 45, 73, or 115 d; all remaining lambs were slaughtered on d 157. Supplementation, with Co-only or VitMin, increased BW at slaughter ( < 0.01), ADG ( < 0.001), carcass weight ( < 0.001), dressing percentage ( < 0.001), carcass fat score ( < 0.05), and the proportion selected for slaughter by d 73 ( < 0.05) and 115 ( < 0.01). Relative to the Control, the benefit to ADG from supplementation increased as the season advanced. Therefore, supplementation did not alter ( = 0.82) ADG between d 1 and 45 but increased ADG over the intervals d 45 to 73 ( < 0.01), d 73 to 115 ( < 0.001), and d 115 to 157 ( < 0.001). There was no difference ( > 0.05) between the Co-only and the VitMin treatments for ADG, carcass weight, fat score, or dressing percentage. Supplementation with Co increased liver Co concentration ( < 0.001), and lambs supplemented with VitMin had greater liver Co concentration than lambs supplemented with Co-only ( < 0.05); the concentrations were 0.18, 0.85, and 1.18 µmol/L for the Control, Co-only, and VitMin treatments, respectively. Treatment had no effect ( = 0.65) on the concentration of Se in kidney tissue. It is concluded that supplementation with Co increased lamb performance after weaning, that response to supplementation increased as the grazing season progressed, and that no extra benefit in performance resulted from augmenting supplementary Co with B and Se.


Subject(s)
Cobalt/pharmacology , Dietary Supplements , Sheep/growth & development , Sodium Selenite/pharmacology , Vitamin B 12/pharmacology , Animals , Body Composition , Cobalt/administration & dosage , Male , Sodium Selenite/administration & dosage , Vitamin B 12/administration & dosage , Vitamins/administration & dosage , Vitamins/pharmacology
2.
Ann Burns Fire Disasters ; 27(3): 146-50, 2014 Sep 30.
Article in English | MEDLINE | ID: mdl-26170794

ABSTRACT

This report describes a case of burn injury following exposure to sulfur mustard, a chemical agent used in war. A review of the diagnostic characteristics, clinical manifestations, and therapeutic measures used to treat this uncommon, yet extremely toxic, entity is presented. The aim of this report is to highlight the importance of considering this diagnosis in any war victim, especially during these unfortunate times of rising terrorist activities.


Ce rapport décrit un cas de brûlure suite à une exposition au gaz moutarde, un agent chimique utilisé dans la guerre. On présente un examen des caractéristiques de diagnostic, les manifestations cliniques et les mesures thérapeutiques utilisés pour traiter ce phénomène rare, mais extrêmement toxique. L'objectif de ce rapport est de mettre en évidence l'importance de considérer ce diagnostic dans toute victime de la guerre, surtout en ces temps malheureux de la hausse des activités terroristes.

3.
Ann Burns Fire Disasters ; 26(1): 16-25, 2013 Mar 31.
Article in English | MEDLINE | ID: mdl-23966894

ABSTRACT

Acute kidney injury (AKI), although rare, is a major complication of burn injury that commonly leads to mortality. It results from a complex interplay of various cellular and neuro-humoral changes affecting burn patients. Guidelines for the treatment of this entity are still not well defined; therefore, prevention and early diagnosis are key to avoid the unfavorable prognosis of AKI. These entail a comprehensive understanding of the global physiologic changes underlying the condition of burn patients and a judicious interpretation of their continuous homeostatic alterations. The aim of this review is to present the salient features in burn patient physiology that contribute to AKI. Strategies for identifying early AKI are presented. Finally, the different treatment modalities are revisited.


Les lésions rénales aiguës (LRA) sont rares, mais elles constituent une complication majeure des brûlures qui mène souvent à la mortalité. Ces lésions sont provoquées par une interaction complexe de divers changements cellulaires et neurohumoraux qui affectent les patients brûlés. Les directives pour le traitement de ces patients ne sont pas encore bien définies et, par conséquent, la prévention et le diagnostic précoce sont essentiels pour éviter le pronostic défavorable des LRA. Cela nécessite une compréhension complète des changements physiologiques présents dans ces patients et une interprétation judicieuse de leurs continuelles altérations homéostatiques. Les Auteurs se sont proposé de présenter les principales caractéristiques de la physiologie du patient brûlé qui contribuent à ce type de lésion. Apres avoir discuté les stratégies pour identifier ces lésions en phase précoce, ils concluent avec une description des différentes modalités de traitement.

4.
J Trauma ; 59(1): 217-22, 2005 Jul.
Article in English | MEDLINE | ID: mdl-16096567

ABSTRACT

BACKGROUND: Although studies have ascertained that ten percent of soldiers killed in battle bleed to death from extremity wounds, little data exists on exsanguination and mortality from extremity injuries in civilian trauma. This study examined the treatment course and outcomes of civilian patients who appear to have exsanguinated from isolated penetrating extremity injuries. METHODS: Five and 1/2 years' data (Aug 1994 to Dec 1999) were reviewed from two Level I trauma centers that receive 95% of trauma patients in metropolitan Houston, TX. Records (hospital trauma registries, emergency medical system (EMS) and medical examiner data) were reviewed on all patients with isolated extremity injuries who arrived dead at the trauma center or underwent cardiopulmonary resuscitation (CPR) or emergency center thoracotomy (ECT). RESULTS: Fourteen patients meeting inclusion criteria were identified from over 75,000 trauma emergency center (EC) visits. Average age was 31 years and 93% were males. Gunshot wounds accounted for 50% of the injuries. The exsanguinating wound was in the lower extremity in 10/14 (71%) patients and proximal to the elbow or knee in 12/14 (86%). Ten (71%) had both a major artery and vein injured; one had only a venous injury. Prehospital hemorrhage control was primarily by gauze dressings. Twelve (86%) had "signs of life" in the field, but none had a discernable blood pressure or pulse upon arrival at the EC. Prehospital intravenous access was not obtained in 10 patients (71%). Nine patients underwent ECT, and nine were initially resuscitated (eight with ECT and one with CPR). Those undergoing operative repair received an average of 26 +/- 14 units of packed red blood cells. All patients died, 93% succumbing within 12 hours. CONCLUSION: Although rare, death from isolated extremity injuries does occur in the civilian population. The majority of injuries that lead to immediate death are proximal injuries of the lower extremities. The cause of death in this series appears to have been exsanguination, although definitive etiology cannot be discerned. Intravenous access was not obtainable in the majority of patients. Eight patients (57%) had bleeding from a site that anatomically might have been amenable to tourniquet control. Patients presenting to the EC without any detectable blood pressure and who received either CPR or EC thoracotomy all died.


Subject(s)
Extremities/injuries , Hemorrhage/mortality , Wounds, Penetrating/mortality , Adolescent , Adult , Child , Female , Humans , Male , Middle Aged , Texas/epidemiology , Trauma Centers
6.
Ann Surg ; 233(5): 603-11, 2001 May.
Article in English | MEDLINE | ID: mdl-11323498

ABSTRACT

OBJECTIVE AND SUMMARY BACKGROUND DATA: Tumor-specific gene therapy can be achieved if a tumor-specific promoter can be identified. In this study the authors investigated the use of the rat insulin promoter (RIP) for insulinoma-specific expression of a reporter gene. Insulinoma-specific cytotoxicity using the suicide gene thymidine kinase (tk) was studied both in vitro and in vivo. RIPtk gene therapy, delivered by a nontoxic, noninflammatory liposomal delivery system, was used in an insulinoma ICR/SCID mouse model to prevent hypoglycemic death. METHODS: Rat insulin promoter (0.502 kb) was ligated to the reporter gene lacZ and ligated to the tk gene. These two genes were transfected into a mouse insulinoma (NIT) cell line to ascertain insulinoma-specific expression and insulinoma-specific cytotoxicity in vitro. Reverse transcriptase-polymerase chain reaction and electrophoretic mobility-shift assays were performed on NIT-1 cell RNA and nuclear extract, respectively, to determine the transcription factors present and responsible for RIP activation in NIT-1 cells. A mouse insulinoma model was created with NIT-1 cells. These mice were treated with the RIPtk gene, and both blood sugars and animal viability were monitored. RESULTS: Only NIT-1 cells stained blue after X-gal staining or had detectable levels of beta-galactosidase protein. A significant decrease in cell survival was observed in NIT-1 cells transfected with RIPtk in vitro. Messenger RNA for both BETA2 and PDX-1 was found in NIT-1 cells, and a supershift was observed for both BETA2 and PDX-1. Experimental mice treated with the RIPtk gene, delivered by a liposomal gene delivery system, maintained their blood glucose levels, and the animals did not die of hypoglycemia. CONCLUSIONS: The data suggest that the RIP is an insulinoma-specific promoter. An ICR/SCID mouse insulinoma model was used to show that insulinoma-specific cytotoxicity can be accomplished by RIP coupled to a suicide gene in vivo, preventing hypoglycemic death.


Subject(s)
Gene Expression Regulation, Neoplastic , Genetic Therapy , Insulinoma/genetics , Insulinoma/therapy , Pancreatic Neoplasms/genetics , Pancreatic Neoplasms/therapy , Animals , Antiviral Agents/therapeutic use , Disease Models, Animal , Female , Ganciclovir/therapeutic use , Lac Operon , Mice , Mice, Inbred ICR , Mice, SCID , Neoplasm Proteins , Nuclear Proteins , Ribosomal Proteins , Transcription, Genetic , Tumor Cells, Cultured
7.
Cell Transplant ; 9(6): 805-15, 2000.
Article in English | MEDLINE | ID: mdl-11202567

ABSTRACT

Gene-targeted mice, derived from embryonic stem cells, are useful tools to study gene function during development. However, if the inactivation of the target gene results in embryonic lethality, the postdevelopmental function of the gene cannot be further studied. The Cre recombinase-loxP (Cre-loxP) system was developed to overcome this limitation as well as to confine the inactivation of the target gene in a cell- or tissue-specific manner. This system allows for the inactivation of the target gene in a single cell type, thereby allowing the analysis of physiological and pathophysiological consequences of the genetic alteration in mature animals. A unique property of the insulin gene to be expressed only in pancreatic beta cells has allowed using the beta-cell-specific rat insulin promoter (RIP) for Cre recombinase expression to inactivate genes in beta cells. The RIP has been used to inactivate genes in beta cells and analysis of these genetically altered mice has provided important information regarding the role of potential transcription factors and the receptors in vivo, for regulation of insulin gene transcription and in the development of beta cells. The Cre-loxP system is at a relatively early stage of development, and the ability of this technique to virtually target any gene in any tissue at any stage of development makes the study of gene function in a single cell type in vivo an attainable goal. It is anticipated that the continued experience with this system will provide an important tool to determine the role of the transcription factors involved in insulin gene regulation and islet cell differentiation and ultimately provide the basis for novel therapy to treat diabetes.


Subject(s)
Gene Silencing , Insulin/genetics , Integrases/genetics , Integrases/metabolism , Islets of Langerhans/physiology , Mice, Transgenic , Viral Proteins , Animals , Genes, Reporter , Humans , Mice , Promoter Regions, Genetic
8.
Pancreas ; 19(4): 346-52, 1999 Nov.
Article in English | MEDLINE | ID: mdl-10547194

ABSTRACT

Islet amyloid polypeptide (IAPP) and insulin are co-stored and generally secreted in parallel; however, studies have demonstrated that the IAPP/insulin molar secretory ratio may be altered in response to certain stimuli. Because we previously demonstrated that intraislet somatostatin is an inhibitory regulator of basal insulin secretion in the isolated perfused human pancreas, this study was designed to determine the relative influence on the regulation of IAPP versus insulin secretion. Single-pass perfusion was performed in pancreata obtained from cadaveric organ donors with continuous perfusion of a modified Krebs media with the glucose level maintained at constant 3.9 mM. Intraislet somatostatin was immunoneutralized by the infusion of either a highly sensitive monoclonal somatostatin antibody (SAb) or its FAb fragment (SFAb). Sequential test periods separated by basal periods were performed by infusion of either of the following: glucose, SAb, SFAb, or appropriate controls. IAPP/insulin molar secretory ratio decreased by 33% in response to infusion of either SAb or the SFAb, respectively (p < 0.01), and decreased by 67% in response to glucose infusion (p < 0.01). An alteration of the IAPP/insulin secretory ratio is seen in response to infusion of exogenous glucose or in response to the neutralization of intraislet somatostatin.


Subject(s)
Amyloid/metabolism , Insulin/metabolism , Pancreas/metabolism , Somatostatin/physiology , Adolescent , Adult , Antibodies, Monoclonal/pharmacology , Cadaver , Child , Female , Glucose/pharmacology , Humans , Immunoglobulin Fab Fragments/pharmacology , Insulin Secretion , Islet Amyloid Polypeptide , Kinetics , Male , Pancreas/drug effects , Somatostatin/antagonists & inhibitors , Tissue Donors
9.
Int J Pancreatol ; 25(3): 157-63, 1999 Jun.
Article in English | MEDLINE | ID: mdl-10453417

ABSTRACT

BACKGROUND: Tissue-specific ablation of a gene using the Cre-loxP system has been used as an important tool to define its role, in addition to the total ablation, to avoid the embryonic lethality in case of wide expression of the target gene. METHODS: The RIP-Cre genetic construct was generated by standard subcloning techniques and microinjected into one cell embryo to develop the transgenic mouse line. Transgenic mice were screened by polymerase chain reaction (PCR) using DNA isolated from tell digestion. Tissue specificity of RIP was demonstrated by transient transfection of RIP-1acZ construct to NIT-1 cells (mouse insulinoma cell line) in vitro. RESULTS: The 448 nucleotides of RIP were sufficient for beta-cell specific expression of the reporter gene as evidenced by the presence of blue color in the nucleus of NIT-1 cells. Isolated RIP-Cre transgene was microinjected, and PCR screening identified two independent lines of transgenic mice. Tissue specificity of RIP was demonstrated by reverse transcriptase polymerase chain reaction (RT-PCR) using the islet RNA from the transgenic mice. CONCLUSION: We have established a tissue-specific transgenic mouse model using Cre recombinase linked to rat insulin promoter (RIP) to drive the expression of the reporter gene specifically in the beta-cells. The RIP-Cre transgenic mice will allow beta-cell specific ablation of target gene(s) to define its role in the regulation of islet physiology.


Subject(s)
Gene Expression , Insulin/genetics , Integrases/genetics , Mice, Transgenic/genetics , Viral Proteins , Animals , Blotting, Southern , Cell Line , Disease Models, Animal , Embryo, Mammalian , Gene Targeting , Liver/metabolism , Mice , Organ Specificity/genetics , Pancreas/metabolism , Promoter Regions, Genetic , Rats , Recombinant Proteins , Reverse Transcriptase Polymerase Chain Reaction , Transfection
10.
J Surg Res ; 84(2): 199-203, 1999 Jun 15.
Article in English | MEDLINE | ID: mdl-10357920

ABSTRACT

Tissue-specific inactivation of a gene using the Cre-loxP system has been used as an important tool to define its role in which the inactivation of the gene in every cell type results in an embryonic lethality. The expression of Cre recombinase (Cre) can be regulated by controlling the timing or spatial distribution of Cre expression via tissue-specific promoters, ligand-inducible promoters, and ligand-dependent Cre fusion proteins. The rat insulin promoter (RIP) has been used in this study to drive the expression of Cre, specifically in the beta cells. The Cre coding sequence was ligated with the RIP and the isolated RIP-Cre transgene was microinjected into one cell embryo to establish a transgenic mouse line. Tissue specificity of the rat insulin promoter was demonstrated by reverse transcriptase polymerase chain reaction using total RNA from pancreas and other tissues of the RIP-Cre transgenic mice. In addition, the efficiency and specificity of RIP was further analyzed by crossbreeding the RIP-Cre transgenic mice with reporter mice bearing a beta-actin-loxP-CAT-loxP-lacZ transgene. In these mice, lacZ is expressed only after excision of the floxed-CAT gene by Cre-mediated recombination. Here, we present the data for beta cell-specific expression of lacZ in the bigenic mice, as proof of concept in a mouse model for targeting beta cell-specific gene(s). The RIP-Cre transgenic mice will be used as a potential tool for targeting the excision of beta cell-specific gene(s) to study their role in islet cell physiology.


Subject(s)
Gene Targeting , Integrases/genetics , Islets of Langerhans/physiology , Viral Proteins , Animals , Gene Expression/physiology , Genes, Reporter/genetics , Insulin/genetics , Lac Operon/genetics , Mice , Mice, Transgenic/genetics , Pancreas/physiology , Promoter Regions, Genetic/genetics , RNA, Messenger/metabolism , Rats , Reverse Transcriptase Polymerase Chain Reaction , Transgenes/genetics
11.
J Laparoendosc Adv Surg Tech A ; 9(2): 147-54, 1999 Apr.
Article in English | MEDLINE | ID: mdl-10235352

ABSTRACT

We report the case of a 31-year-old woman who presented with epigastric pain and weight loss. Esophagogastroduodenoscopy revealed a submucosal mass in the distal antrum and pylorus. Endoscopic biopsy of the mass was nondiagnostic. A CT scan confirmed a 3.0-cm mass in the posterior wall of the distal antrum. She underwent laparoscopic resection of the distal antrum and pylorus with end-to-end gastroduodenostomy. Pathologic examination showed an adenomyoma of the antrum and pylorus. Her postoperative course was uncomplicated, and she continues to do well 38 months postoperatively. Gastric adenomyoma is a rare, benign intramural tumor of the antrum and pylorus. Fewer than 40 cases have been described in the literature. The lesions are generally within 4 cm of the pylorus. Histologically, they are characterized by ductal structures lined by cuboidal to columnar epithelium surrounded by smooth muscle bundles and, occasionally, Brunner's-type glands and heterotopic pancreas. Treatment is by resection, and recurrence has not been reported. Laparoscopic resection of portions of the stomach has been reported. Side-to-side gastrojejunostomies (Billroth II) performed laparoscopically have been reported. This is the first report in the English-language literature of a completely laparoscopically performed sutured gastroduodenostomy. Technical details of the procedure and adenomyomas are discussed.


Subject(s)
Adenomyoma/surgery , Duodenostomy/methods , Gastrostomy/methods , Laparoscopy , Stomach Neoplasms/surgery , Suture Techniques , Adenomyoma/pathology , Adult , Anastomosis, Surgical/methods , Female , Humans , Pyloric Antrum , Stomach Neoplasms/pathology , Surgical Stapling
12.
Surgery ; 124(2): 254-8; discussion 258-9, 1998 Aug.
Article in English | MEDLINE | ID: mdl-9706146

ABSTRACT

BACKGROUND: Recently five somatostatin receptor subtypes (SSTRs) were cloned, allowing the development of highly specific agonists to these SSTRs. Previous studies have shown a species specificity phenomenon with respect to the inhibition of insulin secretion by these selective agonists. This study was undertaken to determine which SSTR (2 or 5) is responsible for the inhibitory effect of somatostatin on glucose-stimulated mouse insulin secretion. METHODS: Intact mouse islets (n = 10) were stimulated with D-glucose in the presence or absence of receptor-specific somatostatin agonists. RESULTS: D-glucose (16.7 mmol/L) augmented insulin secretion by 158% above that seen with 3.9 mmol/L D-glucose. In the presence of DC 32-92 (SSTR5) selective agonist, D-glucose (16.7 mmol/L) augmented insulin secretion by 64% above that seen with 3.9 mmol/L D-glucose. The presence of SSTR 5 selective agonist resulted in a significant (P < .05) inhibition of glucose-stimulated insulin secretion. The identification of SSTR5 within the mouse pancreas was established by reverse transcriptase polymerase chain reaction and confirmed by Southern blot analysis. CONCLUSIONS: These results suggest that the inhibitory effect of somatostatin on insulin secretion is mediated through the subtype 5 receptor within the mouse islet.


Subject(s)
Insulin/metabolism , Islets of Langerhans/chemistry , Islets of Langerhans/metabolism , Receptors, Somatostatin/metabolism , Animals , Blotting, Southern , Dose-Response Relationship, Drug , Glucose/pharmacology , Insulin Secretion , Islets of Langerhans/drug effects , Male , Mice , Mice, Inbred Strains , Organ Culture Techniques , Polymerase Chain Reaction , RNA, Messenger/analysis , Receptors, Somatostatin/agonists , Receptors, Somatostatin/genetics
13.
Biochem Biophys Res Commun ; 253(1): 65-9, 1998 Dec 09.
Article in English | MEDLINE | ID: mdl-9875221

ABSTRACT

The rat insulin promoter (RIP) has been used to drive the expression of Cre recombinase (Cre) specifically in beta cells. Transient transfection was performed in the mouse insulinoma cell line, NIT-1, and control cell lines. RT-PCR was performed using total RNA from pancreas and other tissues of RIP-Cre transgenic mice. In addition, the efficiency and specificity of RIP were further analyzed by cross breeding the RIP-Cre transgenic mice with reporter mice bearing a beta-actin-loxP-CAT-loxP-lacZ transgene. In these mice, lacZ is expressed only after excision of the floxed-CAT gene by Cre-mediated recombination. Here, we present the data for beta cell-specific expression of lacZ in bigenic mice, as proof of concept in a mouse model for targeting beta cell-specific gene(s). The RIP-Cre transgenic mice will be used as a potential tool for targeting the excision of beta cell-specific gene(s) to study their role in islet cell physiology.


Subject(s)
Gene Targeting/methods , Integrases/genetics , Islets of Langerhans/metabolism , Viral Proteins , Animals , Cell Line , Crosses, Genetic , Gene Expression Regulation , Genes, Reporter , Insulin/genetics , Insulinoma , Islets of Langerhans/physiology , Lac Operon , Mice , Mice, Transgenic , Promoter Regions, Genetic , Rats , Reverse Transcriptase Polymerase Chain Reaction , Transfection , Transgenes , beta-Galactosidase/genetics
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