Hematologic variables : hematocrit, hemoglobin concentration and reticulocyte count in pugs and French bulldogs

Brakycefala hundraser är ofta drabbade av brakycefalt obstruktivt syndrom vilket kan ge en nedsatt syresättning. Brakycefala hundar kan jämföras med människor drabbade av sömnapné och engelsk bulldog har därför använts som studiemodell för dessa patienter. Det är sedan tidigare konstaterat att människor med sömnapné har högre hemoglobinkoncentration och hematokrit jämfört med friska kontroller. Förhöjda hemoglobinkoncentrationer och hemtokriter som fysiologisk anpassning till syrebrist har även hävdats kunna drabba brakycefala hundar även om specifika studier för att undersöka detta aldrig har utförts. Syftet med denna studie var att undersöka om brakycefala hundar har förhöjda hemoglobinkoncetrationer och hematokriter. I studien användes data från mopsar och franska bulldoggar vilka jämfördes med en kontrollgrupp med hundar av liknande storlek och vikt. Journaluppgifter togs från hundar blodprovstagna på någon av följande fyra kliniker: SLU Universitetsdjursjukhuset, Anicura Albano; Bagarmossen eller Roslagen. Totalt inkluderades 118 stycken mopsar, 148 stycken franska bulldoggar och 164 stycken i kontrollgruppen. De franska bulldoggarna hade signifikant högre hemoglobinkoncentration och hematokrit jämfört med kontrollgruppen medan mopsarna hade signifikant lägre hemoglobinkoncentration och hematokrit. Mopsarna hade däremot signifikant högre retikulocytantal jämfört med kontrollgruppen och ingen skillnad kunde för detta visas mellan de franska bulldoggarna och kontrollgruppen. Fåtalet skillnader påvisades när de olika klinikerna, könen och åldrarna jämfördes inom och mellan grupperna. Studien diskuterar möjliga förklaringar till dessa förändringar hos de brakycefala hundarna så som ålder, underliggande sjukdom och normalvariation för raserna. Vissa är mer sannolika än andra men sammanfattningsvis konstateras det att inte alla brakycefala hundar har förhöjd hematokrit och hemoglobinkoncentration.Brachycephalic dogs are often affected by brachycephalic obstructive airway syndrome, which can result in a decreased oxygenation. These dogs can be compared to people diagnosed with obstructive sleep apnea. One study even used the English bulldog as a study model for these patients. It has already been stated that people with sleep apnea have increased levels of hemoglobin and hematocrit compared to a healthy control group. With this reasoning similar differences have been suggested to apply to brachycephalic dogs even though there’s no studies specifically studying this. The purpose of this study was to confirm or refute these statements. This study used data from pugs and French bulldogs that were compared to a control group consisting of dogs with a similar weight and size. Information from medical records was collected from the following four clinics: SLU Universitetsdjursjukhuset, Anicura; Albano; Bagarmossen and Roslagen. In total 118 pugs, 148 French bulldogs and 164 in the control group were included in the study. For the French bulldogs it was concluded that their hemoglobin concentration and hematocrit was significantly higher than the control group but for the pug-group both hemoglobin concentration and hemoglobin was significantly lower. Few differences were found when the different clinics, genders and ages were compared within and between all groups. Multiple explanations to these changes are discussed in the following study for example age, underlying disease and breed variation. Some are more likely than others but to conclude it cannot be stated that all brachycephalic dog breeds suffer from increased hematocrit and hemoglobin concentration

A descriptive study of regular parturition and dystocia in dogs

Hundavel ökar i popularitet och att ha en god förståelse för hur normal dräktighet och förlossning går till är därför viktigt. Syftet med denna litteraturstudie är att beskriva det normala i förhållande till när det uppstår komplikationer under förlossning. Tikar blir könsmogna vid sex till nio månaders ålder när dem genomgår sin första östruscykel. Ägglossningen sker under östrus och äggen befruktas i äggledaren för att efter ett antal dagar implanteras i livmodern. Dräktigheten varar i 63 dagar från ovulation men en stor spridning ses. Under en normal förlossning kan valpar och moderkakor förlösas om vart annat och det är viktigt att hålla koll på durationen för förlossningen för att minska antalet komplikationer. Faktorer bakom dystoki kan delas in i maternella och fetala anledningar. Exempel på maternella anledningar är värksvaghet och anatomiska avvikelser. Värksvaghet är den vanligaste anledning till dystoki. Värksvaghet definieras som misslyckandet för livmodern att inducera förlossning och kan bero på att antalet foster är för få eller för många. Anatomiska avvikelser är svåra att diagnosticera och upptäcks oftast inte förrän det är försent. Fetala anledningar orsakar obstruktiv dystoki och kan ha överdimensionerade foster och foster i fellägen som bakgrund. Behandling av dystoki kan göras både medicinskt och kirurgiskt. Oxytocin och kalcium är vanliga substanser som används men om dessa inte är tillräckliga kan kejsarsnitt vara indikerat. Riskfaktorer som tagits upp och har störst betydelse för dystoki är rastillhörighet, storlek på tiken och kullstorlek.Dog breeding is becoming increasingly popular and to possess good knowledge of normal pregnancy and parturition is therefore important. The purpose of this literature study is to describe what’s normal in relation to when complications occur during parturition. Bitches reach sexual maturity when they are six to nine months old. The start of their sexual maturity is when they go through their first oestrus cycle. Ovulation occurs during the oestrus-phase and the eggs are fertilized in the fallopian tubes. After approximately a week the eggs are implanted in the uterus. The pregnancy lasts for 62-64 days after ovulation however there is a large spread in gestation length. During normal parturition puppies and placentas can be delivered alternately and it’s important to keep track of the duration of the parturition to avoid complications. Factors leading up to dystocia can be divided in to two subgroups: maternal and fetal. Examples of maternal causes are uterine inertia and anatomical anomalies. Uterine inertia is the most common cause of dystocia and is defined as the uterine failure to induce parturition. The presence of too few or too many fetuses is a contributing factor to uterine inertia. Anatomical anomalies are hard to diagnose and is therefore often detected too late. The fetal causes behind dystocia are often obstructive and due to oversized fetuses or fetal malpresentation. Dystocia can be treated both medically and by surgery. Oxytocin and calcium are two components who are often administered as a medical treatment but if they’re not enough a caesarean section may be indicated. Risk factors which have been discussed in this study as most relevant to cause dystocia are litter size, the size of the bitch and what breed the bitch is

Ansvar och kemiska vapen - En argumentationsanalys om kemiska vapen bör tolkas in i Responsibility to Protect

De kemiska vapenattackerna i Syrien har lett oss till att undra om det internationella samfundets ansvar att ingripa. Vi har därför undersökt om kemiska vapen bör tolkas in i de situationer där Responsibility to Protect kan tillämpas. Med hjälp av en argumentationsanalys har vi jämfört argumentationen om kemiska vapen med fyra brott som har antagits av FN att falla under kriterierna av situationer som kan sätta R2P i verkan. Det visades att kemiska vapen kunde tolkas in i två av dessa fyra brott: krigsbrott och brott mot mänskligheten. Vi har diskuterat utifrån teorin om rättfärdigt krig, med fokus på jus in bello, om just kemiska vapen borde tolkas in. Vi har dragit slutsatsen att kemiska vapen har hamnat i en subkategori till andra brott och måste lyftas upp till en principiell övergripande nivå för att specifikt tolkas in som ett eget brott på grund av dess obestridliga kränkning mot krigets lagar

Pituitary Adenylate Cyclase Activating Peptide (1-38) and its analog (Acetyl-[Ala15, Ala20] PACAP 38-polyamide) reverse methacholine airway hyperresponsiveness in rats

O objetivo deste estudo foi investigar funcionalmente e estruturalmente efeito broncodilatador do peptídeo ativador da adenilato ciclase pituitária (PACAP1-38) e da acetil-[Ala15, Ala20]PACAP 38-poliamida, potente análogo do PACAP-38, nos ratos desafiados pelo metacolina (MeCh). Ratos Wistar machos foram aleatoriamente divididos em cinco grupos. Grupos 1 e 2, inalando aerossóis de solução salina ou doses crescentes de MeCh (0,5, 1, 2,12, 4,25, 8,5, 17, 34 e 68 mg/L). Os outros grupos recebendo terbutalina (Terb) (250 µg/rato) (10-6M), PACAP-38 (50 µg/rato) (0.1 mM) ou análogo do PACAP-38 (50 µg/rato) associados a MeCh na dose de 4,25 mg/L. A resistência pulmonar total (RL) foi registrada antes e 2 min após a administração de Mech pelo equipamento pneumomultiteste. A administração MeCh induziu aumento significativo e dose dependente (pThe aim of this study was to investigate both functionally and structurally bronchodilator effects of Pituitary adenylate cyclase activating peptide (PACAP38) and acetyl-[Ala15, Ala20] PACAP38-polyamide, a potent PACAP38 analog, in rats challenged by methacholine (MeCh). Male Wistar rats were divided randomly into five groups. Groups 1 and 2 inhaled respectively aerosols of saline or increasing doses of MeCh (0.5, 1, 2.12, 4.25, 8.5, 17, 34 and 68mg/L). The other groups received terbutaline (Terb) (250 µg/rat) (10-6 M), PACAP38 (50 µg/rat) (0.1 mM) or PACAP38 analog (50 µg/rat) associated to MeCh from the dose of 4.25 mg/L. Total lung resistances (RL) were recorded before and 2 min after MeCh administration by pneumomultitest equipment. MeCh administration induced a significant and a dose-dependent increase (

Evaluation of the BOADICEA risk assessment model in women with a family history of breast cancer

The ability of the Breast and Ovarian Analysis of Disease Incidence and Carrier Estimation Algorithm (BOADICEA) model to predict BRCA1 and BRCA2 mutations and breast cancer incidence in women with a family history of breast cancer was evaluated. Observed mutations in 263 screened families were compared to retrospective predictions. Similarly, observed breast cancers in 640 women were compared to retrospective predictions of breast cancer incidence. The ratios of observed to expected number of BRCA1- , BRCA2- and BRCA(1 or 2) mutations were 1.43 (95% CI 1.05–1.90), 0.63 (95% CI 0.34–1.08), and 1.12 (95% CI 0.86–1.44), showing a significant underestimation of BRCA1 mutations. Discrimination between carriers and non-carriers as measured by area under the receiver operating characteristic (ROC) curve was 0.83 (95% CI 0.76–0.88). The ratio of observed to expected number of invasive breast cancers was 1.41 (0.91–2.08). The corresponding area under the ROC curve for prediction of invasive breast cancer at individual level was 0.62 (95% CI 0.52–0.73). In conclusion, the BOADICEA model can predict the total prevalence of BRCA(1 or 2) mutations and the incidence of invasive breast cancers. The mutation probability as generated by BOADICEA can be used clinically as a guideline for screening, and thus decrease the proportion of negative mutation analyses. Likewise, individual breast cancer risks can be used for selecting women whose risk of breast cancer indicates follow-up. Application of local mutation frequencies of BRCA1 and BRCA2 could improve the ability to distinguish between the two genes

Downregulation of peroxisome proliferator-activated receptors (PPARs) in nasal polyposis

BACKGROUND: Peroxisome proliferator-activated receptor (PPAR) α, βδ and γ are nuclear receptors activated by fatty acid metabolites. An anti-inflammatory role for these receptors in airway inflammation has been suggested. METHODS: Nasal biopsies were obtained from 10 healthy volunteers and 10 patients with symptomatic allergic rhinitis. Nasal polyps were obtained from 22 patients, before and after 4 weeks of local steroid treatment (fluticasone). Real-time RT-PCR was used for mRNA quantification and immunohistochemistry for protein localization and quantification. RESULTS: mRNA expression of PPARα, PPARβδ, PPARγ was found in all specimens. No differences in the expression of PPARs were obtained in nasal biopsies from patients with allergic rhinitis and healthy volunteers. Nasal polyps exhibited lower levels of PPARα and PPARγ than normal nasal mucosa and these levels were, for PPARγ, further reduced following steroid treatment. PPARγ immunoreactivity was detected in the epithelium, but also found in smooth muscle of blood vessels, glandular acini and inflammatory cells. Quantitative evaluation of the epithelial immunostaining revealed no differences between nasal biopsies from patients with allergic rhinitis and healthy volunteers. In polyps, the PPARγ immunoreactivity was lower than in nasal mucosa and further decreased after steroid treatment. CONCLUSION: The down-regulation of PPARγ, in nasal polyposis but not in turbinates during symptomatic seasonal rhinitis, suggests that PPARγ might be of importance in long standing inflammations

Presymptomatic cognitive and neuroanatomical changes in genetic frontotemporal dementia in the Genetic Frontotemporal dementia Initiative (GENFI) study: a cross-sectional analysis.

BACKGROUND: Frontotemporal dementia is a highly heritable neurodegenerative disorder. In about a third of patients, the disease is caused by autosomal dominant genetic mutations usually in one of three genes: progranulin (GRN), microtubule-associated protein tau (MAPT), or chromosome 9 open reading frame 72 (C9orf72). Findings from studies of other genetic dementias have shown neuroimaging and cognitive changes before symptoms onset, and we aimed to identify whether such changes could be shown in frontotemporal dementia. METHODS: We recruited participants to this multicentre study who either were known carriers of a pathogenic mutation in GRN, MAPT, or C9orf72, or were at risk of carrying a mutation because a first-degree relative was a known symptomatic carrier. We calculated time to expected onset as the difference between age at assessment and mean age at onset within the family. Participants underwent a standardised clinical assessment and neuropsychological battery. We did MRI and generated cortical and subcortical volumes using a parcellation of the volumetric T1-weighted scan. We used linear mixed-effects models to examine whether the association of neuropsychology and imaging measures with time to expected onset of symptoms differed between mutation carriers and non-carriers. FINDINGS: Between Jan 30, 2012, and Sept 15, 2013, we recruited participants from 11 research sites in the UK, Italy, the Netherlands, Sweden, and Canada. We analysed data from 220 participants: 118 mutation carriers (40 symptomatic and 78 asymptomatic) and 102 non-carriers. For neuropsychology measures, we noted the earliest significant differences between mutation carriers and non-carriers 5 years before expected onset, when differences were significant for all measures except for tests of immediate recall and verbal fluency. We noted the largest Z score differences between carriers and non-carriers 5 years before expected onset in tests of naming (Boston Naming Test -0·7; SE 0·3) and executive function (Trail Making Test Part B, Digit Span backwards, and Digit Symbol Task, all -0·5, SE 0·2). For imaging measures, we noted differences earliest for the insula (at 10 years before expected symptom onset, mean volume as a percentage of total intracranial volume was 0·80% in mutation carriers and 0·84% in non-carriers; difference -0·04, SE 0·02) followed by the temporal lobe (at 10 years before expected symptom onset, mean volume as a percentage of total intracranial volume 8·1% in mutation carriers and 8·3% in non-carriers; difference -0·2, SE 0·1). INTERPRETATION: Structural imaging and cognitive changes can be identified 5-10 years before expected onset of symptoms in asymptomatic adults at risk of genetic frontotemporal dementia. These findings could help to define biomarkers that can stage presymptomatic disease and track disease progression, which will be important for future therapeutic trials. FUNDING: Centres of Excellence in Neurodegeneration

Diagnosis and treatment of brain metastases from solid tumors: guidelines from the European Association of Neuro-Oncology (EANO)

The management of patients with brain metastases has become a major issue due to the increasing frequency and complexity of the diagnostic and therapeutic approaches. In 2014, the European Association of Neuro-Oncology (EANO) created a multidisciplinary Task Force to draw evidence-based guidelines for patients with brain metastases from solid tumors. Here, we present these guidelines, which provide a consensus review of evidence and recommendations for diagnosis by neuroimaging and neuropathology, staging, prognostic factors, and different treatment options. Specifically, we addressed options such as surgery, stereotactic radiosurgery/stereotactic fractionated radiotherapy, whole-brain radiotherapy, chemotherapy and targeted therapy (with particular attention to brain metastases from non-small cell lung cancer, melanoma and breast and renal cancer), and supportive care

Presymptomatic cognitive and neuroanatomical changes in genetic frontotemporal dementia in the Genetic Frontotemporal dementia Initiative (GENFI) study: A cross-sectional analysis

Background: Frontotemporal dementia is a highly heritable neurodegenerative disorder. In about a third of patients, the disease is caused by autosomal dominant genetic mutations usually in one of three genes: progranulin (. GRN), microtubule-associated protein tau (. MAPT), or chromosome 9 open reading frame 72 (. C9orf72). Findings from studies of other genetic dementias have shown neuroimaging and cognitive changes before symptoms onset, and we aimed to identify whether such changes could be shown in frontotemporal dementia. Methods: We recruited participants to this multicentre study who either were known carriers of a pathogenic mutation in GRN, MAPT, or C9orf72, or were at risk of carrying a mutation because a first-degree relative was a known symptomatic carrier. We calculated time to expected onset as the difference between age at assessment and mean age at onset within the family. Participants underwent a standardised clinical assessment and neuropsychological battery. We did MRI and generated cortical and subcortical volumes using a parcellation of the volumetric T1-weighted scan. We used linear mixed-effects models to examine whether the association of neuropsychology and imaging measures with time to expected onset of symptoms differed between mutation carriers and non-carriers. Findings: Between Jan 30, 2012, and Sept 15, 2013, we recruited participants from 11 research sites in the UK, Italy, the Netherlands, Sweden, and Canada. We analysed data from 220 participants: 118 mutation carriers (40 symptomatic and 78 asymptomatic) and 102 non-carriers. For neuropsychology measures, we noted the earliest significant differences between mutation carriers and non-carriers 5 years before expected onset, when differences were significant for all measures except for tests of immediate recall and verbal fluency. We noted the largest Z score differences between carriers and non-carriers 5 years before expected onset in tests of naming (Boston Naming Test -0·7; SE 0·3) and executive function (Trail Making Test Part B, Digit Span backwards, and Digit Symbol Task, all -0·5, SE 0·2). For imaging measures, we noted differences earliest for the insula (at 10 years before expected symptom onset, mean volume as a percentage of total intracranial volume was 0·80% in mutation carriers and 0·84% in non-carriers; difference -0·04, SE 0·02) followed by the temporal lobe (at 10 years before expected symptom onset, mean volume as a percentage of total intracranial volume 8·1% in mutation carriers and 8·3% in non-carriers; difference -0·2, SE 0·1). Interpretation: Structural imaging and cognitive changes can be identified 5-10 years before expected onset of symptoms in asymptomatic adults at risk of genetic frontotemporal dementia. These findings could help to define biomarkers that can stage presymptomatic disease and track disease progression, which will be important for future therapeutic trials. Funding: Centres of Excellence in Neurodegenerati