Brief discussion on prevention of the secondary damage in the procedures of D2 lymphadenectomy for gastric cancer / 中华胃肠外科杂志

So far, D2 lymphadenectomy has been recognized as the key one of the procedures in curative resection for gastric cancer. In summary, the standardized implementation of D2 lymphadenectomy can contribute to both surgical quality and patients′ prognosis. Lymph node dissection, as an important basis for local surgical treatment of gastric cancer, involves certain technical risks due to complex adjacent relationship and anatomical variation of organs or blood vessels, and so on. There is a certain incidence of side injuries in D2 lymphadenectomy for a surgeon, regardless of the experience of learning curve. Complying with specification of surgical procedures and summarizing the vital points of lymph node dissection in each curative gastrectomy for gastric cancer is the principal method to reduce or avoid the occurrence of relevant complications after surgery.

Inflammatory response and anti-inflammatory therapy after acute spinal cord injury / 中国药理学通报

Acute spinal cord injury can lead to severe motor,sen-sory and sphincter muscle dysfunction.Inflammatory response caused by inflammatory cytokines plays a crucial role in the oc-currence and development of secondary damage.Maintaining the body balance between inflammaion and anti-inflammation through an appropriate anti-inflammatory intervention will be an important strategy for drug therapy of spinal cord injury.This paper mainly introduces the cause,process and participation of inflammatory response in the pathophysiological mechanism of acute spinal cord injury,and also reviews the latest progress of experimental research of anti-inflammatory drugs,aiming to provide reference for finding the safe and effective drugs.

Potential Biological Mechanism Underlying Rehabilitation Training after Spinal Cord Injury (review) / 中国康复理论与实践

Spinal cord injury is a kind of disease with high disability rate and poor prognosis. According to the degree of injury and damage plane, adopting appropriate rehabilitation measures can effectively enhance the patient's sensory and motor function, and ultimately improve the quality of life. This article briefly introduced the content of rehabilitation training corresponding with various periods, and sum-marized that relieving the secondary injury, improving the regenerative microenvironment, promoting proliferation and differentiation of en-dogenous neural stem cells differentiation and inducing plasticity were the biological mechanisms underlying the effect of rehabilitation training.

Pathophysiology of neurodegeneration following traumatic brain injury / Patofisiología de la neurodegeneración tras una lesión traumática del cerebro

Acute neuropathological conditions, including brain and spinal cord trauma, are leading causes of death and disabilities worldwide, especially in children and young adults. The causes of brain and spinal cord injuries include automobile accidents, accidents during recreational activities, falls and violent attacks. In the United States of America alone, around 1.7 million people each year seek medical care for some kind of head injury. About fifty-two thousand of these people will die, while the same number will present with permanent functional disability. Considering the high worldwide prevalence of these acute pathological conditions, research on the mechanisms underlying central nervous system damage is of extreme importance. Nowadays, a number of experimental models of acute neural disorders have been developed and the mechanisms of tissue loss have been investigated. These mechanisms include both primary and secondary pathological events contributing to tissue damage and functional impairment. The main secondary pathological mechanisms encompass excitotoxicity, ionic imbalances, inflammatory response, oxidative stress and apoptosis. The proper elucidation of how neural tissue is lost following brain and spinal cord trauma is fundamental to developing effective therapies to human diseases. The present review evaluates the main mechanisms of secondary tissue damage following traumatic brain and spinal cord injuries.

Las condiciones neuropatológicas agudas, incluyendo los traumas del cerebro y la médula espinal, se hallan entre las principales causas de muerte y discapacidades a nivel mundial, sobre todo en niños y adultos jóvenes. Las causas de las lesiones del cerebro y la médula espinal, incluyen los accidentes automovilísticos, accidentes en actividades recreativas, caídas y ataques violentos. Sólo en los Estados Unidos de Norte América, alrededor de 1.7 millones de personas buscan anualmente atención médica para algún tipo de lesión craneal. Cincuenta y dos mil de estas personas morirán, mientras que un número similar presentará alguna discapacidad funcional permanente. Dada la alta prevalencia de estas condiciones patológicas agudas a nivel mundial, la investigación de los mecanismos que subyacen en los daños al sistema nervioso central, constituye un asunto de suma importancia. Hoy día, se han desarrollado varios modelos experimentales de trastornos neurales agudos, y se han investigado los mecanismos de la pérdida de tejido. Estos mecanismos incluyen tanto las manifestaciones patológicas primarias como las secundarias, que contribuyen al daño del tejido y al deterioro funcional. Los mecanismos patológicos secundarios principales abarcan la excitotoxicidad, los desequilibrios iónicos, la respuesta inflamatoria, el estrés oxidativo, y la apoptosis. Dilucidar correctamente como ocurre la pérdida del tejido neuronal luego del trama del cerebro o la médula espinal, es fundamental para poder desarrollar terapias efectivas en relación con las enfermedades humanas. La presente revisión evalúa los mecanismos principales del daño secundario al tejido, tras las lesiones traumáticas del cerebro y la médula espinal.

Perihematoma Damage at Different Time Points in Experimental Intracerebral Hemorrhage / 华中科技大学学报（医学）（英德文版）

The damage degree of neurons in perilesion at different time points was observed in order to explore the optimal operation occasion. Piglet lobar hematomas were produced by pressure-controlled infusions of 2.5 mL autonomous blood into the right frontal hemispheric white matter over 15 min, and the metabolic changes were ambulatorily detected with MRS at 3rd, 12th, 24th and 48th h after hematoma induction. Brain tissues of perihematoma were also obtained at different time points. The transcription level of Bax gene was detected by in situ hybridization and apoptosis by TUNEL technique, and the pathologic change of neurons was observed under an electron microscope. The results showed that the number of Bax positive cells reached the peak at 24 h (79.00±4. 243/5 fields). There was no significant difference in A values between 3 h and 6 h, 12 h (P＞0.05), but there significant difference between 24 h and 3 h, 6 h, 12 h (P＜0.05). The number of apoptotic cells reached the peak at 24 h (P＜0. 001), and there was no significant difference betw een 3 h and 6 h (P=0. 999). The area of the apoptotic cells showed no significant difference between 3 h and 6 h or among 3 h, 6 h and 6 h (P＞0.05). Lac peak mainly occurred at 24 h and 48 h, while on the healthy side, no Lac peak was detectable. The ratio of NAA/Cr presented a descent tendency, but there was no significant difference among the groups before 12 h (P＞0.05), there was very significant difference between 3, 6 and 24, 48 h (P＜0.01). Under electronic microscopy, the neuronal damage surrounding hematoma in 3 to 6 h was milder than in 24 h to 48 h. It was concluded that the secondary apoptosis, damage and metabolic disturbance of the neurons surround ing hematoma was milder in 3-6 h in acute intracerebral hemorrhage, while obviously aggravated in 24-48 h. An effective intervention is needed to reduce secondary damage as soon as possible.

Pathophysiology of Craniocerebral Trauma

In the past decade, major advances have been made in defining and, to some extent, quantifying the types of brain damage that occur in non-missile head injury, and in identifying their pathogenesis, using biological models of head injury. There have been various approaches to the classification of brain damage and we have tended to emphasize the existence of primary and secondary damage from impairment of cerebral blood flow and brain metabolism, which helps in the identification of at least potentially preventable complications.