Dengue Virus Infects Primary Human Hair Follicle Dermal Papilla Cells

During the epidemic of the dengue virus (DENV) infection in Taiwan in 2014 and 2015, we observed an abnormally high frequency of increased scalp hair shedding in infected individuals that could not be explained by telogen effluvium. In this study, the mechanism of hair loss caused by DENV was explored. Human hair follicle dermal papilla cells (HFDPCs) are essential for hair follicle morphogenesis and cycling. Thus, we established an in vitro DENV infection model in HFDPCs. On immunofluorescence analysis, HFDPCs that were susceptible to DENV infection responded to type I interferon (IFN) treatment, and the cells showed antibody-dependent enhancement (ADE) effect. The expression of the pro-inflammatory cytokines, interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-α), revealed an inflammatory response in DENV-infected HFDPCs. In particular, DENV infection impaired cell viability, and it activated caspase-associated cell death signaling in HFDPCs. In conclusion, our data indicate that direct infection with DENV causes inflammation and cell death in HFDPCs, which is involved in the mechanisms of hair loss after DENV infection. The knowledge of DENV infection in an immune-privileged tissue, such as hair follicles, may suggest their use for further studies on post-dengue fatigue syndrome (PDFS)

Acute Paraparesis Caused by a Giant Cell Tumor of the Thoracic Spine

AbstractGiant cell tumor (GCT) is a benign but locally aggressive skeletal neoplasm of young adults. GCT located in the spine is relatively rare and may need a combination of surgical and adjunctive therapies. Here we present a patient who had intermittent thoracic back pain for two weeks and experienced an acute episode of decreased muscle power of both lower limbs. Magnetic resonance (MR) imaging examinations of the thoracic spine revealed that the patient had severe spinal canal compression caused by pathological fracture due to a tumor within the seventh thoracic vertebra. She underwent an emergent surgical intervention for total removal of the tumor and spinal reconstruction with autologous rib grafts and instruments. Postoperatively, the patient made an uneventful recovery of muscle power of bilateral lower limbs. She subsequently received adjuvant radiotherapy. In a follow-up period of 36 months, the patient had no clinical or radiological evidence of tumor recurrence. Even though spinal location for GCT is a rare event, it should be included in the differential diagnosis in patients with osteolytic lesions or pathological fractures of the vertebra, especially in young female patients sustaining no trauma who had a clinical history of persistent low back pain

Increased spinal prodynorphin gene expression in reinflammation-associated hyperalgesia after neonatal inflammatory insult

<p>Abstract</p> <p>Background</p> <p>Neuroplasticity induced by neonatal inflammation is the consequence of a combination of activity-dependent changes in neurons. We investigated neuronal sensitivity to a noxious stimulus in a rat model of neonatal hind-paw peripheral inflammation and assessed changes in pain behaviour at the physiological and molecular levels after peripheral reinflammation in adulthood.</p> <p>Results</p> <p>A decrease in paw withdrawal latency (PWL) after a heat stimulus was documented in rats that received inflammatory injections in their left hind paws on postnatal day one (P1) and a reinflammation stimulus at postnatal 6-8 weeks of age, compared with normal rats. An increase in the expression of the prodynorphin (<it>proDYN</it>) gene was noted after reinflammation in the spinal cord ipsilateral to the afferents of the neonatally treated hind paw. The involvement of the activation of extracellular signal-regulated kinases (ERK) in peripheral inflammatory pain hypersensitivity was evidenced evident by the increase in phospho-ERK (pERK) activity after reinflammation.</p> <p>Conclusions</p> <p>Our results indicate that peripheral inflammation in neonates can permanently alter the pain processing pathway during the subsequent sensory stimulation of the region. Elucidation of the mechanism underlying the developing pain circuitry will provide new insights into the understanding of the early pain behaviours and the subsequent adaptation to pain.</p