https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37272 Wed 16 Sep 2020 14:03:32 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50107 Wed 12 Jul 2023 13:43:56 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:1059 Wed 11 Apr 2018 14:05:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30004 Wed 11 Apr 2018 12:27:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10193 Wed 11 Apr 2018 12:07:24 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36077 Haemophilus influenzae is the most commonly identified bacteria. Haemophilus influenzae is divided into typeable and nontypeable (NTHi) strains based on the presence or absence of a polysaccharide capsule. While NTHi is a common commensal in the human nasopharynx, it is associated with considerable inflammation when it is present in the lower airways of COPD patients, resulting in morbidity due to worsening symptoms and increased frequency of COPD exacerbations. Treatment of lower airway NTHi infection with antibiotics, though successful in the short term, does not offer long-term protection against reinfection, nor does it change the course of the disease. Hence, there has been much interest in the development of an effective NTHi vaccine. This review will summarize the current literature concerning the role of NTHi infections in COPD patients and the consequences of using prophylactic antibiotics in patients with COPD. There is particular focus on the rationale, findings of clinical studies and possible future directions of NTHi vaccines in patients with COPD.]]> Wed 09 Feb 2022 15:54:02 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47644 Tue 24 Jan 2023 14:44:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19823 Tue 09 Jun 2020 09:48:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30788 Thu 27 Jan 2022 15:58:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7929 Sat 24 Mar 2018 08:41:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9594 Sat 24 Mar 2018 08:39:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7639 Sat 24 Mar 2018 08:36:02 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9647 Sat 24 Mar 2018 08:35:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:6919 1.0 mm) primary melanoma. It was 18 and 17.3 in subcutaneous and lymph node metastases, respectively (P < 0.0001). GRP78 expression was positively correlated with increasing tumour thickness (P = 0.001) and with increasing dermal tumour mitotic index (P = 0.0004). Disease-free survival (χ² = 8.0703, P = 0.0045) and overall survival (χ² = 6.2633, P = 0.0123) in melanoma patients with IRS >25 were significantly lower than in melanoma patients with IRS <25. Conclusions: GRP78 expression appears to correlate with known correlates of melanoma progression and survival and requires further evaluation as a prognostic biomarker in melanoma.]]> Sat 24 Mar 2018 08:34:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7261 Sat 24 Mar 2018 08:33:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13695 1. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals^2,3, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk⁴. Modestly powered genome-wide association studies (GWAS)^5-10 have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility¹¹. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis.]]> Sat 24 Mar 2018 08:19:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21279 Sat 24 Mar 2018 07:54:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:360 Sat 24 Mar 2018 07:42:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54017 Mon 29 Jan 2024 13:26:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34150 Mon 23 Sep 2019 12:33:00 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34156 Mon 18 Mar 2019 11:44:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34154 S. mansoni produces less severe intestinal pathology than that reported from Egypt. In the rest of Africa the disease is still milder. MANSON-BAHR [13] reported that symptomatology in East Africa due to S. mansoni infection was variable but noted that, in general, the infected indigenous population was symptom-free. Although WYDELL [19] demonst rat ed severe intestinal pathology in the later stages of S . mansoni infection in an isolated African population group on Ukerewe Island in Lake Victoria, and although t he incidence of S . mansoni in this group was high, he noted that intestinal symptoms in active infections were uncommon. Further south, GELFAND [8] from S. Rhodesia report ed that intestinal bilharziasis is almost asymptomatic and he stressed the benign nature of the intestinal lesions. Little work has been done on the clinico-pathological aspects of intestinal bilharziasis in South Africa. TURNER [18] reported that symptoms due to intestinal bilharziasis were variable and were easily mist aken for chronic diarrhoea or t dysentery. HOLLAND [9] considered bilharzial dysentery to be a rare illness. KING [11] reported on the similarities in clinical presentation of amoebiasis and bilharzial dysentery. SCHNEIDER [11] reported that , when present, symptoms were mild in the Transvaal African.]]> Mon 18 Mar 2019 11:37:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38890 Fri 25 Feb 2022 17:03:28 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34155 Schistosomes, mansoni and haematobium, in which the manifestations of bilharzial disease are but slight by comparison with the distribution of the parasites. The third well-known form of bilharzia, due to Schistosoma japonicum, is in a slightly different position for here there cannot be much doubt as to the disease-producing potential of some strains of this particular parasite.]]> Fri 15 Feb 2019 16:33:39 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41804 Fri 12 Aug 2022 12:31:50 AEST ]]>