Tag Archives: ephrin receptor

Despite of progress in various computational methods on

Despite of progress in various computational methods on evaluating the success of various MHC-peptide binding prediction, there is no consensus on a perfect method. However, in this study, ProPred and ProPred-I servers discovered a lot of HLA-A, HLA-B, HLA-C (MHC class I proteins) and HLA-DR (MHC class II) restricted epitopic fractions from full-length QD protein. ProPred or ProPred-I recognized that QD protein could bind to several different types of HLA ephrin receptor which could trigger immune response. In the next step, comparative analysis of the continuous B-cell epitope results and predicted T-cell restricted epitopes showed several T-cell epitopes derived from B-cell binding sequences from QD protein which possibly will evoke strong both humoral and cell-mediated immune responses. The two peptide sequences of QD antigen, “AYHKGNWSGYGKDGNIGIKDEDGMNCGPIAGSCTFPTTGTSKSPSPFVDLGAKDATSG” and “GPIAGSCTFPTTGTSKSPSP” possessed these properties. In this study, E. coli BL21 (DE3) strain as suitable prokaryotic expression system could express heterologous QD protein. In this study, the E. coli BL21 (DE3) strain showed significant expression after 6–8 h of induction at 37 °C. There was no toxic effect of QD protein on the E. coli BL21 cells. The poly-histidine-tag sequence efficiently helped the purification of QD by Ni2+-affinity chromatography method. Our antigen remains to be tested for the immunological efficacy.
Several regions of QD recombinant protein from P. aeruginosa were found to be efficient antigens. Almost all conserved QD antigenic patches were enriched with irregular coil and turn motif. Our predictions showed that the QD chimeric protein with several T-cell epitopes derived from B-cell epitopes could be expressed efficiently in E. coli BL21 (DE3) strain and could serve as a good subunit of vaccine candidate against P. aeruginosa.

Conflict of interest statement

Acknowledgments

Introduction
The external ventricular drain (EVD) constitutes a clinical standard for the continuous monitoring of intracranial pressure (ICP) and facilitates the drainage of cerebrospinal fluid (CSF). Indications for an EVD include primary hydrocephalus, obstructive hydrocephalus secondary to expansive processes or intracranial haemorrhage, ICP control in patients with cranioencephalic trauma and prevention of postoperative CSF fistulas[1,2]. It facilitates the treatment using intraventricular fibrinolysis (IVF) and the administration of local antibiotics[1,3]. Its indications are limited by the risk of bleeding during the insertion procedure and the risk of ventriculostomy-related infection (VRI)[1–6]. The published indication on the VRI seems to be conflicting since incidence rates vary between 0% and above 50% depending on the authors[1,2,4–10]. There are no universal criteria to establish its diagnosis; strategies focus on clinical monitoring and blood and CSF microbiological and citobiochemical results[1,2,4,6–14]. The clinical assessment of the patient and certain test results that suggest infection (leucocytosis, CSF pleocytosis, hypoglycorrhachia, etc.) lose their predictive value due to the particular characteristics of the neurocritical patient[15–17], and they can cause delay in its detection and early treatment; the lack of rentability of the cultures and the fact that waiting is needed for their results to be available are also obstacles to an early diagnosis[18,19].
The need to establish uniform criteria which are both highly sensitive and specific for the diagnosis of VRI seems necessary, and, also, to determine CSF parameters to predict its development[12]. The etiological agent most commonly involved is the coagulase-negative staphylococci[1,2,11–13,18,20], however, the detected amount of Gram-negatives is increasing. Many factors that could contribute to the development of VRI have been identified (associated craniotomy, systemic infection, depressed cranial fracture, intraventricular haemorrhage, catheter manipulation, and instillation of local treatments)[1,2,4,11,13,14,21,22], whereas some others are subjects of continuous debate (use of prophylactic antibiotics, the number of devices, corticosteroids administration, lengthy stays in critical care units, placement site of the catheter, prophylactic replacement of the catheter, duration of the derivation, etc.)[1,4,14,20–28].

ephrin receptor There were several limitations to this

There were several limitations to this study. The sample was a volunteer rather than a representative sample, so care must be made in generalizing these results to the wider ephrin receptor with lower limb arthritis. The limited number of health conditions used as exclusion criteria means that some participants with arthritis may have had other health problems contributing to their balance impairment. In addition, the control group participants did not undergo rigorous screening of their health status, so some may have had subclinical health problems that might have affected their balance performance. The use of 12-month retrospective falls recall may have resulted in under-reporting of falls. There is a higher proportion of women with arthritis in the community,1 and gender effects have been previously demonstrated on some balance and mobility related tasks,44 therefore, the study sample was restricted to females. A similar study involving men with arthritis is warranted.
5. Conclusions
The results of this study demonstrated high risk of falls and balance and mobility impairment in older women with OA and RA. There were some differences in falls circumstances, and falls risk factor profile between these two groups, highlighting the importance of falls risk assessment in people with OA or RA. However, on most balance and mobility tasks, both groups of arthritis participants demonstrated similar increased levels of impairment across several balance domains. Given the moderate levels of balance impairment identified, future research should investigate the effectiveness of balance exercise programs, and multifactorial falls prevention programs, addressing identified falls risk factors, for older people with OA or RA.
Acknowledgments
Funding: J. O. and J. R. Wicking Trust, managed by ANZ Trustees.
1. Introduction
Neurocysticercosis (NCC) is a common parasitic infection of the human central nervous system caused by pork tapeworm Taenia solium. NCC is a serious public health problem in several developing countries in Latin America, Asia and Africa. It is well known that NCC, the commonest parasitic brain disease,1 causes epilepsy, focal neurological signs, intracranial hypertension, stroke and neuropsychiatry symptoms.2,3 We report a case of an elderly person presented with rapidly progressive dementia as the isolated manifestation of multiple NCC.
2. Case report
A 65-year-old right-handed male, postgraduate and clerk by profession, presented with occipital headache which was moderate to severe in intensity with occasional bouts of vomiting of 4 months\’ duration and a gradual progressive decline in cognitive functions of 3 months\’ duration. Initially he had problem in performing his professional work. He had great difficulty in calculation and made mistakes in his files, had difficulty in comprehension of paragraphs, forgot information, and misplaced objects and files. He was unable to supervise his children\’s studies and often lost his temper and responsed with irritability. There was marked slowness in doing daily activity and thought processes, lack of spontaneity, apathy, and lack of interest toward the environment and himself. Gradually he became unconcerned about his personal hygiene, forgot to eat meals, and got lost in new places. He was unable to recall his address, telephone numbers, or names of close relatives within a span of three months. His cognitive decline was severe enough to impair his personal and occupational performance. His symptoms were observed by his wife and reported to our hospital.

S V T S V

S34-V1569853207 2007-273T13:44:55-13:46:20 36 18 120 23.1 47.8 9.4 35.9 ??10.4 183882.
S34-V1569853808 2007-273T13:54:56-13:56:21 36 18 120 23.0 48.7 9.3 36.8 ??10.4 187928.
S34-V1569854409 2007-273T14:04:57-14:06:22 36 18 120 22.9 49.5 9.2 37.7 ??10.4 191945.
S34-V1569854506 2007-273T14:06:34-14:07:59 36 18 120 22.9 49.7 9.2 37.9 ??10.4 192744.
S34-V1569854700 2007-273T14:09:48-14:11:13 36 18 120 22.8 50.0 9.2 38.3 ??10.4 194339.
S70-V1696219767 2011-275T03:19:40-03:20:56 34 17 120 28.8 102.7 0.0 129.4 11.4 199816.
S70-V1696219855 2011-275T03:21:08-03:22:24 34 17 120 28.8 102.8 0.0 129.5 11.4 199916.
S70-V1696219943 2011-275T03:22:36-03:23:52 34 17 120 28.7 103.0 0.0 129.6 11.4 200017.
Table options
Table 5.
Rhea disk-integrated observations processed in this ephrin receptor work. Columns S and L indicate the cube dimensions along sample and lines axis, respectively.
SEQUENCE START-END S L EXP PHASE SUBSPC SUBSPC SSOL SSOL SPC ALT
OBS ID TIME (UT) (s) (°) LON (°) LAT (°) LON (°) LAT (°) (km)
S17-V1516202693 2006-017T14:55:22-14:56:28 42 36 40 34.7 309.1 0.3 338.7 ??18.5 226163.
S17-V1516202765 2006-017T14:56:34-14:57:40 42 36 40 34.8 309.0 0.3 338.8 ??18.5 225845.
S43-V1597403216 2008-227T10:28:30-10:30:00 32 16 160 27.7 348.9 ??4.1 321.2 ??5.3 1638460.
S43-V1597403307 2008-227T10:30:01-10:31:30 32 16 160 27.7 348.9 ??4.1 321.3 ??5.3 1638800.
S43-V1597404177 2008-227T10:44:31-10:46:01 32 16 160 27.4 349.4 ??3.9 322.1 ??5.3 1642060.
osteoporosis S43-V1597405905 2008-227T11:13:19-11:14:49 32 16 160 26.9 350.4 ??3.7 323.7 ??5.3 1648300.
S43-V1597405996 2008-227T11:14:50-11:16:19 32 16 160 26.9 350.5 ??3.7 323.8 ??5.3 1648620.
S43-V1597406099 2008-227T11:16:33-11:18:03 32 16 160 26.8 350.5 ??3.7 323.9 ??5.3 1648990.
S43-V1597407060 2008-227T11:32:34-11:34:04 32 16 160 26.5 351.1 ??3.6 324.8 ??5.3 1652310.
S43-V1597407151 2008-227T11:34:05-11:35:34 32 16 160 26.5 351.2 ??3.6 324.8 ??5.3 1652610.
S43-V1597407254 2008-227T11:35:48-11:37:18 32 16 160 26.5 351.2 ??3.6 324.9 ??5.3 1652970.
S43-V1597407345 2008-227T11:37:19-11:38:48 32 16 160 26.4 351.3 ??3.6 325.0 ??5.3 1653270.
S43-V1597407448 2008-227T11:39:02-11:40:32 32 16 160 26.4 351.3 ??3.6 325.1 ??5.3 1653620.
S43-V1597407539 2008-227T11:40:33-11:42:02 32 16 160 26.4 351.4 ??3.6 325.2 ??5.3 1653920.
S43-V1597407642 2008-227T11:42:16-11:43:01 32 16 80 26.3 351.4 ??3.6 325.3 ??5.3 1654200.
S43-V1597407688 2008-227T11:43:02-11:43:46 32 16 80 26.3 351.5 ??3.5 325.3 ??5.3 1654350.
S43-V1597407740 2008-227T11:43:54-11:44:39 32 16 80 26.3 351.5 ??3.5 325.4 ??5.3 1654530.
S43-V1597407786 2008-227T11:44:40-11:45:24 32 16 80 26.3 351.5 ??3.5 325.4 ??5.3 1654680.
S43-V1597407838 2008-227T11:45:32-11:46:17 32 16 80 26.3 351.6 ??3.5 325.5 ??5.3 1654850.
S43-V1597407884 2008-227T11:46:18-11:47:02 32 16 80 26.3 351.6 ??3.5 325.5 ??5.3 1655000.
S43-V1597407936 2008-227T11:47:10-11:47:55 32 16 80 26.3 351.6 ??3.5 325.5 ??5.3 1655180.

The present study demonstrated that

The present study demonstrated that there was a correlation between higher FCP levels and NEC occurrence in the case group; this is in agreement with Albanna et al.,16 who found significantly higher FCP levels in neonates who developed NEC, with maximum level in neonates with Bell\’s stage IIIb (307.6?±?4.1), which was also in agreement with Aydemir et al.,17 who found that raised FCP can predict the occurrence of NEC, as mean FCP concentrations in NEC cases (185?mg/dL) were significantly higher than controls (104?mg/dL). Also, they found that there was a significant positive correlation between NEC severity and FCP level. Yoon et al.15 also found that FCP concentration was higher in newborns with NEC than controls. El Fragy et al.29 showed that FCP can be used as a non-invasive marker for early prediction of NEC in neonates.
In a study by Thuijls et al. that involved 35 neonates suspected of NEC, 14 of them developed NEC. Median of FCP levels together with urinary intestinal fatty ephrin receptor binding protein and claudin-3 were significantly higher in neonates with NEC than in neonates with other diagnoses, with a cut-off level of FCP (286.2?μg/g feces).30 Carroll et al. showed that FCP was markedly elevated – with a mean concentration of 288.4?mg/L – in patients with NEC, compared to 98.0?mg/L in controls.22 FCP was increased to >2000?μg/g in three cases of NEC and in one case of covered perforation with microscopic bowel inflammation.25
All of the 52 studied neonates were under treatment with antibiotics, so we were not able to identify the effect of postnatal antibiotics on FCP level. Fecal samples were not always easily obtainable in infants who had feeding intolerance, as they had delayed gastric emptying, and also during stop feeding duration it was difficult to take a stool sample.
It was concluded that preterm with feeding intolerance had statistically significant elevated levels of FCP compared to preterm infants without feeding intolerance.
Conflicts of interest
The authors declare no conflicts of interest.