Bacterial contamination of computer touch screens.

The goal of this study was to determine the occurrence of opportunistic bacterial pathogens on the surfaces of computer touch screens used in hospitals and grocery stores. Opportunistic pathogenic bacteria were isolated on touch screens in hospitals; Clostridium difficile and vancomycin-resistant Enterococcus and in grocery stores; methicillin-resistant Staphylococcus aureus. Enteric bacteria were more common on grocery store touch screens than on hospital computer touch screens.

Peripheral nerve stimulation for trigeminal neuropathic pain.

Facial pain is a complex disease with a number of possible etiologies. Trigeminal neuropathic pain (TNP) is defined as pain caused by a lesion or disease of the trigeminal branch of the peripheral nervous system resulting in chronic facial pain over the distribution of the injured nerve. First line treatment of TNP includes management with anticonvulsant medication (carbamazepine, phenytoin, gabapentin, etc.), baclofen, and analgesics. TNP, however, can be a condition difficult to adequately treat with medical management alone. Patients with TNP can suffer from significant morbidity as a result of inadequate treatment or the side effects of pharmacologic therapy. TNP refractory to medical management can be considered for treatment with a growing number of invasive procedures. Peripheral nerve stimulation (PNS) is a minimally invasive option that has been shown to effectively treat medically intractable TNP. We present a case series of common causes of TNP successfully treated with PNS with up to a 2 year follow-up. Only one patient required implantation of new electrode leads secondary to electrode migration. The patients in this case series continue to have significant symptomatic relief, demonstrating PNS as an effective treatment option for intractable TNP. Though there are no randomized trials, peripheral neuromodulation has been shown to be an effective means of treating TNP refractory to medical management in a growing number of case series. PNS is a safe procedure that can be performed even on patients that are not optimal surgical candidates and should be considered for patients suffering from TNP that have failed medical management.

Sacral nerve stimulation as a treatment modality for intractable neuropathic testicular pain.

BACKGROUND: Chronic testicular pain, or "chronic orchalgia," is defined as testicular pain 3 months or longer in duration that significantly interferes with the daily activities of the patient. For patients failing to respond to conservative treatment, microsurgical denervation of the spermatic cord, epididymectomy, and vasovasostomy have all shown a degree of relief. However, these are all invasive procedures and no treatment has proven efficacy when these options fail. We present a case of a male who presented with over a decade of chronic right-sided testicular pain secondary to recurrent epididymitis. Before arriving at our clinic the patient had an epididymectomy performed with no appreciable improvement in pain. Initially ilioinguinal, iliohypogastric, and genetofemoral nerve blocks; right-sided S1, S2, and S3 transforaminal epidural steroid injections (TFESIs) with inferior hypogastric blocks; and right-sided T12-L1, L1-L2, and L2-L3 TFESIs all failed to provide pain relief. After conservative therapies had failed, a sacral nerve stimulation trial was done via a caudal epidural approach. The permanent implant has provided the patient with sustained 80% decrease in pain at 4 months status post permanent sacral nerve stimulation implant. The above case demonstrates the potential benefit of sacral nerve stimulation with neuropathic intractable testicular pain in a patient that failed conservative treatment. In this case, the patient had exhausted medical and surgical management, including advanced interventional pain options. We were unable to find any previous published cases of neurostimulation used as a modality of treatment for testicular pain, and further studies are needed to gain a better understanding of the efficacy in this setting.

A role for calcium-calmodulin in regulating nitric oxide production during skeletal muscle satellite cell activation.

When skeletal muscle is stretched or injured, myogenic satellite cells are activated to enter the cell cycle. This process depends on nitric oxide (NO) production by NO synthase (NOS), matrix metalloproteinase activation, release of hepatocyte growth factor (HGF) from the extracellular matrix, and presentation of HGF to the c-met receptor as demonstrated by a primary culture and in vivo assays. We now add evidence that calcium-calmodulin is involved in the satellite cell activation cascade in vitro. Conditioned medium from cultures that were treated with a calcium ionophore (A23187, ionomycin) for 2 h activated cultured satellite cells and contained active HGF, similar to the effect of mechanical stretch or NO donor treatments. The response was abolished by addition of calmodulin inhibitors (calmidazolium, W-13, W-12) or a NOS inhibitor N(G)-nitro-l-arginine methyl ester hydrochloride but not by its less inactive enantiomer N(G)-nitro-d-arginine methyl ester hydrochloride. Satellite cells were also shown to express functional calmodulin protein having a calcium-binding activity at 12 h postplating, which is the time at which the calcium ionophore was added in this study and the stretch treatment was applied in our previous experiments. Therefore, results from these experiments provide an additional insight that calcium-calmodulin mediates HGF release from the matrix and that this step in the activation pathway is upstream from NO synthesis.