Rapid Detection of Staphylococcus aureus Using Graphene Oxide Coated Screen-Printed Sensor Strips

340–343Staphylococcus aureus (S. aureus) is the most common reason behind bacterial infections in humans. They cause a wide array of infections on skin, bone and joint medical implants and blood stream. In order to mitigate these infections, detecting the presence of this bacterium is of prime importance. This paper explores a new rapid detection technique to identify S aureus bacteria. A screen-printed sensor coated with graphene oxide was used as an identification platform. Graphene oxide was synthesized using modified Hummer’s method and was characterized using X-ray Diffractometer and Scanning Electron Microscope. The developed sensors showed significant decrease in the bulk resistance with the increase in bacterial concentrations. The developed sensors were subjected to selectivity, repeatability and reusability tests and showed good results

Rapid Detection of Staphylococcus aureus Using Graphene Oxide Coated Screen-Printed Sensor Strips

Staphylococcus aureus (S. aureus) is the most common reason behind bacterial infections in humans. They cause a wide array of infections on skin, bone and joint medical implants and blood stream. In order to mitigate these infections, detecting the presence of this bacterium is of prime importance. This paper explores a new rapid detection technique to identify S aureus bacteria. A screen-printed sensor coated with graphene oxide was used as an identification platform. Graphene oxide was synthesized using modified Hummer’s method and was characterized using X-ray Diffractometer and Scanning Electron Microscope. The developed sensors showed significant decrease in the bulk resistance with the increase in bacterial concentrations. The developed sensors were subjected to selectivity, repeatability and reusability tests and showed good results

Clinical spectrum of stiff person syndrome associated with glutamic acid decarboxylase antibodies

Objective: The aim of this study was to examine the clinical characteristics and associated diagnosis of the SPS. Background: Stiff person syndrome (SPS) is an immune-mediated neurological disorder that can cause rigidity of the axial and limb muscles. About 80% of patient with SPS have had high-titer antibodies against glutamic acid decarboxylase (GAD), and 15% have antibodies to glycine receptors. Design/Methods: Retrospective chart review of patients with SPS and positive GAD antibody who were seen over 5 years was performed. Demographics, detailed clinical information, and diagnostic data were recorded. Coexisting autoimmune diseases and serologies were reviewed. Results: Nine patients were included in this study, 7 women and 2 men. The median age at symptom onset was 47 years. Six patients had positive Gad antibody and 3 were negative. Primary diagnosis was stiff person syndrome (n=4), cerebellar ataxia (n=2), PERM (n=2) and sensory neuropathy/neuronopathy (n=1). Commonly associated antibodies were islet cell antibody and neuronal voltage-gated potassium channel. Type 1 diabetes, seizures, and thyroid disease were commonly associated with the diagnosis. Three patients had an EMG finding suggestive of SPS and two of these patients had negative GAD antibody. Conclusions: Women are commonly affected by the disease. There is a phenotypic variation of the disease as previously reported in the literature. EMG is helpful in the diagnosis of negative GAD antibody patients where clinical suspicion for SPS is high

Ustekinumab related CIDP in a patient with psoriatic arthritis

Objective: To describe a case of ustekinumab related CIDP. Background: Ustekinumab is an IL- 12/23 monoclonal antibody recently approved for psoriatic arthritis, plaque psoriasis and Crohn\u27s disease. There are several reports of association between anti-TNF-alpha antagonists and a variety of cases of PNS demyelination. However, none have been yet documented with ustekinumab. Design/Methods: Case report. Results: A 52 year-old man with history of psoriatic arthritis presented with subacute onset of ascending quadriparesis and paresthesias of the arms and legs two weeks after starting ustekinumab, rendering him nonambulatory without assistance. Examination showed moderate quadriparesis, diffuse areflexia, and decreased pinprick in the arms and legs. CSF showed albuminocytologic dissociation and was otherwise unremarkable. EMG showed evidence for non-length dependent diffuse demyelinating sensorimotor neuropathy of the arms and legs. Workup including ANA, RF, cryoglobulin, DNA, SSA, SSB, cANCA, pANCA, Scl-70, HIV, GM1 Ab, thiamine, B6, vitamin B12, hepatitis B/C, TSH, complement, C. jejuni, porphyrin, Lyme Ab, vitamin E, and copper was negative or normal. Patient received 5 PLEX sessions with dramatic improvement in strength with residual numbness of lower extremities. Nine days later he had recurrence of ascending weakness with numbness to the point that he could not ambulate without a walker. Repeat EMG was consistent with diagnosis of CIDP. He received 5 additional PLEX sessions with improvement of his symptoms except for residual numbness of his hands and legs. He continued outpatient PLEX weekly then every 2 weeks after which he had another relapse with similar presentation of marked weakness. He remained PLEX dependent for 6 months after onset of symptoms and was gradually weaned off. He has remained minimally symptomatic with normal strength, mild recrudescence of reflexes and stable residual numbness on mycophenolate monotherapy. Conclusions: This is the first known case report of ustekinumab related CIDP. More research is needed to establish a causal relationship

Using local GND density to study SCC initiation

In this work, strain and geometric necessary dislocations (GNDs) have been mapped with nm-resolution around grain boundaries affected by stress corrosion cracking (SCC) or intergranular oxidation with the aim of clarifying which local conditions trigger SCC initiation.Comment: 36 pages, 19 figure

Value of terminal latency index and sensory electrophysiology in idiopathic and diabetic chronic inflammatory demyelinating polyradiculoneuropathy

Objectives: To evaluate sensory electrophysiology, terminal latency index (TLI), and treatment response in idiopathic and diabetic chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Methods: We performed a retrospective review of 147 patients with CIDP who underwent electrodiagnostic evaluation (January 2000–December 2015). Eighty-nine patients fulfilled electrophysiological criteria described by the Ad hoc Subcommittee of the American Academy of Neurology and Albers et al. Fifty-eight patients were divided into idiopathic (N = 40) and diabetic (N = 18) groups. These groups were compared for age, sex, cerebrospinal fluid protein, response to treatment, sensory response abnormalities, and TLI measurements using chi-square tests for binary and categorical variables and using t-tests and mixed-effects models for continuous variables. Results: The difference in abnormal rates of sensory responses was significant for the sural nerve, with the idiopathic group having a lower rate than the diabetic group (80% vs. 100%, p \u3c 0.001). No group differences in the TLI measurements were significant. Conclusions: Sural sensory responses may have some value in differentiating idiopathic CIDP from diabetic CIDP. Larger prospective studies are needed to confirm our findings. Significance: Our study suggests that abnormal sural sensory potentials may have some significance in differentiating idiopathic CIDP from diabetic CIDP