Successful resuscitation and multidisciplinary management of penetrating brain injury caused by tire explosion: A case report.

RATIONALE: Penetrating brain injury (PBI) is a rare trauma that presents as a difficult and serious surgical emergency for neurosurgeons in clinical practice. Our patient was admitted with a PBI caused by a tire explosion, which is an extremely rare cause of injury. PATIENT CONCERNS: We report a case of a 28-year-old male patient who suffered a PBI when a tire exploded while it was being inflated with a high-pressure air pump. DIAGNOSES: The patient was diagnosed with PBI presenting with multiple comminuted skull fractures, massive bone fragments with foreign bodies penetrating the underlying brain tissue of the top right frontal bone, multiple cerebral contusions, and intracranial hematoma. INTERVENTIONS: Emergency combined multidisciplinary surgery was performed for the removal of the fragmented bone pieces, hematoma, and foreign bodies; decompression of the debridement flap; reconstruction of the anterior skull base; and repair of the dura mater. OUTCOMES: The patient was successfully resuscitated and discharged 1 month later and is now recovering well. LESSONS: Patients with PBI are critically ill. Therefore, timely, targeted examinations and appropriate multidisciplinary interventions through a green channel play a key role in assessing the condition, developing protocols, and preventing complications.

HCV inhibits M2a, M2b and M2c macrophage polarization via HCV core protein engagement with Toll-like receptor 2.

Hepatitis C virus (HCV) establishes a persistent infection in most patients, eventually leading to chronic hepatitis C (CHC), cirrhosis and hepatocellular carcinoma. Our previous study revealed that HCV core protein (HCVc) inhibited the differentiation of monocytes into M1 and M2 macrophages. However, it remains unclear as to whether HCVc affects the polarization of M2 macrophages, and if this effect promotes the progression of chronic disease. In the present study, peripheral blood mononuclear cells (PBMCs) from patients with CHC and healthy controls (HCs) were isolated, purified and polarized to M2a, M2b and M2c macrophages. Phenotypic expression, cytokine secretion and gene expression were analyzed using flow cytometry, ELISA and reverse transcription-quantitative polymerase chain reaction, respectively. Monocytes from HCs were cultured with HCVc to study the effect of HCVc on macrophage polarization. Plasma alanine transaminase and HCV-RNA levels were significantly higher, and albumin levels were significantly lower in the CHC group than those in the control group (P<0.05). M2a macrophages polarized from monocytes of patients with CHC expressed lower levels of CD209, IL-1 receptor antagonist (IL-1RA) and Fizz1 compared with those from HCs. M2b macrophages expressed lower levels of CD86 and TNF-α, and M2c macrophages expressed lower levels of CD163, TGF-ß and sphingosine kinase 1 (SPHK1) in the CHC group compared with HCs (P<0.05). HCVc inhibited the expression levels of CD209, IL-1RA and Fizz1 in M2a macrophages; CD86 and TNF-α in M2b macrophages; and CD163, TGF-ß and SPHK1 in M2c macrophages (P<0.05). HCVc significantly suppressed phagocytosis of all subtypes (P<0.05); however, this inhibition was restored by an anti-Toll-like receptor (TLR)2 antibody (P<0.05). In conclusion, HCVc inhibited monocyte-derived M2a, M2b and M2c subtype differentiation via the TLR2 signaling pathway, resulting in macrophages exhibiting reduced phagocytosis in patients with CHC. This may contribute to persistent HCV infection, thus suggesting that the blockade of HCVc may be a new therapeutic approach for the treatment of HCV infection.

Protective effects of scopolamine and penehyclidine hydrochloride on acute cerebral ischemia-reperfusion injury after cardiopulmonary resuscitation and effects on cytokines.

The objective of this study was to investigate the protective effects of scopolamine and penehyclidine hydrochloride on acute cerebral ischemia-reperfusion injury after cardiopulmonary resuscitation, and the effect on cytokine levels. Eighty patients with cardiac arrest admitted to our hospital from June 2011 to December 2015 were recruited and randomly divided into two groups (n=40 each). Following cardiopulmonary resuscitation, scopolamine was administered in the control group, whereas penehyclidine hydrochloride was administered in the observation group. After intervention, the following medical indicators were compared between the groups: Intracranial pressure, cerebral oxygen partial pressure, cerebral perfusion pressure, assessment of the balance of cerebral oxygen supply and demand, levels of neuron-specific enolase (NSE) and blood lactic acid, levels of oxidative stress markers, and levels of inflammatory-related factors. Additionally, the areas of brain tissue edema and National Institutes of Health Stroke Scale (NIHSS) scores before and after intervention were compared. Rescue success rates of the groups were recorded. After intervention, the following indicators were lower in the observation group than in the control group: Intracranial pressure (p<0.05), levels of NSE (p<0.05), levels of blood lactic acid (p<0.05), levels of malondialdehyde (p<0.05), and levels of interleukin 6 (IL-6), tumor necrosis factor-α, IL-1, and hs-CRP (p<0.05). However, the following indicators were higher in the observation group than in the control group: Cerebral oxygen partial pressure, cerebral perfusion pressure (p<0.05), levels of CaO2, CjvO2, and CERO2 (p>0.05), and levels of superoxide dismutase and glutathione peroxidase (p<0.05). Additionally, the areas of brain tissue edema after intervention were smaller in the observation group than those before intervention and those after intervention in the control group (p<0.05). Similarly, the NIHSS scores after intervention in the observation group were lower than those before intervention and those after intervention in the control group (p<0.05). Rescue success rate was significantly higher in observation group than in control group (p<0.05). In conclusion, administration of penehyclidine following cardiopulmonary resuscitation can effectively improve cerebral perfusion pressure, lower intracranial pressure, reduce brain tissue edema and inflammation, and improve neurological function.