ObjectiveTo investigate the clinical characteristics of motorcycle spoke heel injury and the effectiveness of sequential therapy of vacuum sealing drainage (VSD) and pedicled flap transplantation for treating motorcycle spoke heel injury in children. MethodsBetween January 2010 and January 2014, 15 children (aged from 3 to 8 years, 5.7 years on average) with motorcycle spoke heel injury received sequential therapy of VSD and pedicled flap transplantation. The interval from injury to admission was 3-7 days, with an average of 4.9 days. The locations were the heel in 8 cases, the heel and lateral malleolus in 2 cases, and the medial malleolus and medial heel in 4 cases, and the medial and lateral malleolus and heel in 1 case. The patients had different degrees of defects of the skin, tendon, and bone. The skin defect size ranged from 3 cm×3 cm to 13 cm×6 cm. VSD was applied for twice in 13 cases and three times in 2 cases. Reversed flow sural flap was applied in 8 cases, lateral supramalleolar flap in 2 cases, medial supramalleolar perforator-based flaps in 4 cases, and posterior tibial artery flap in 1 case. Eight pedicled flaps with neuroanastomosis were selected according to the wound characteristics. The flap size ranged from 4 cm×4 cm to 14 cm×7 cm. ResultsOf 15 cases, 13 flaps survived well except that two had partial skin necrosis at the distal site. Primary healing was obtained, and skin graft at donor site survived. The patients were followed up 9-21 months (mean, 13 months). Mild and moderate bulky flaps were observed in 9 cases and 6 cases respectively. Of 15 cases, 13 could walk with weight loading, and 2 had slight limping. Superficial sensation recovered to S3 in 8 patients undergoing neuroanastomosis, and recovered to S2 in 7 patients not undergoing neuroanastomosis at 6 months after operation. According to AOFAS evaluation system for Ankle-Hindfoot, the results were excellent in 13 cases and good in 2 cases, with an excellent and good rate of 100% at 8 months after operation. ConclusionThe main characteristic of motorcycle spoke heel injury lies in a combination of high energy damage and thermal damage. Sequential therapy of VSD and pedicled flap transplantation can be regarded as a reliable option to obtain good outcome of wound healing and satisfactory functional recovery for the management of motorcycle spoke heel injury.
Rheumatoid arthritis (RA) is one of the most common chronic inflammatory diseases. It mainly involves joints, as well as extra-articular organs. The extra-articular manifestations (EAM) are more common in patients with severe active disease, and the mortality of RA patients with EAM is 2.5 times of RA patients without EAM. Renal damage is rare in EAM, which mainly includes renal damage associated with RA itself, renal amyloidosis, and drug-induced secondary renal damage. In recent years, researches on RA renal damage have gradually increased, and mainly focused on therapy and prognosis. The recent research progress of RA renal damage are summarized in this review.
In order to observe activity of tumor necrosis factor (TNF) in the serum, pancreatic histopathological damage, as well as their relationships in acute necrotizing pancreatitis (ANP), thirty five SD rats were randomly divided into 7 groups according to their sampling time with 5 in each group. ANP was induced by retrograde infusion of 5% sodium taurocholate through biliopancreatic duct in 6 experimental groups (Group B1～B6).Blood and pancreatic tissue samples were obtained at hour 0,0.5,2,4,6 or 8 respectively when the animals were sacrificed.Results showed that serum level of TNF activity rose significantly in Group B2,and reached the maximal value in Group B4.The pancreatic histopathological damage in ANP rats was getting worse along with time. Serum TNF activity had close relation to pancreatic histopathological score (r=0.63, Ｐ＜0.01),suggesting that serum TNF may play an important role in the process of deterioration of pancreatic tissue damage during ANP.
Objective To determine the efficacy of D980-nm laser in dissolving fat and renewing skin, and to explore the clinical application of D980-nm laser in reconstruction of photodamaged skin. Methods Eighteen 12-14 month-old male Sprague-Dawley rats, weighing 400-450 g, were randomly divided into 3 groups (n=6). The rat skin at the left side was exposed to D980-nm laser irradiation at a density of 20 J/cm2, a power of 8 W, a pulse width of 20 ms, and a pulse frequency of 40 Hz for 1 time (group A), 2 times of 5-minute interval (group B), and 3 times of 5-minute interval (group C) as a treatment course, for 4 treatment courses with an interval of 1 week; the other side of the skin was not treated as the control groups (groups A1, B1, and C1, respectively). After 8 weeks, the skin was harvested for HE staining and immunohistochemical staining to observe the structure changes of skin, to measure the dermal thickness, to count the number of fibroblasts, and detect the expressions of transforming growth factor β1 (TGF-β1) and basic fibroblast growth factor (bFGF). Results Compared with groups A1, B1, and C1, the skin structure was significantly improved in groups A, B, and C. After D980-nm laser irradiation, the number of fat cells decreased; local angiogenesis was observed; the total number of fibroblasts and fibers increased; the collagen fiber had large diameter, and arranged closely and regularly; the dermal thickness and the number of the fibroblasts increased; and the expressions of TGF-β1 and bFGF were significantly enhanced, showing significant differences (P<0.05). With increased D980-nm laser irradiation times, the above indexes increased, showing significant differences between group C and groups A, B (P<0.05). Conclusion D980-nm laser treatment has lipolytic and tender effect on the skin, and the frequency of the treatment is an important factor in skin renewal.
ObjectiveTo explore the application value of damage control in intra-abdominal sepsis. MethodsThe related literatures were searched by searching literatures with " damage control” " damage control resuscitation” damage control surgery”, and " intra-abdominal sepsis”, to made an review. Results Despite significant advances in management and treatment, mortality from intra-abdominal sepsis remained still high. Due to its unique anatomic and microbial environment, initial operation could not completely remove the source of infection and avoid complications. Therefore, it was becoming increasingly popular to utilize a damage control strategy with abbreviated laparotomy and planned reoperations. ConclusionsDamage control is characterized by staged treatment, and is widely accepted used to manage intra-abdominal sepsis.
Aminoadipic acid(AAA) is known to damage retinal glia cells primarily when it is given to animals intravitreally. The present study is to demonstrate marked increase of retinal susceptibility to photic damage following administration of sub-thres-hold doses of this agent to albino rats. Right eyes were intravitreally injected with 10 ?l of 10 mM AAA, a dose which caused transient swelling of Muller cell nucleiimmediately after treatment, and total recovery by 24 hours. These rats were exposed to fluorescent light at 150 f.c. for one hour three days after injection. The left eyes were injected with the same amount of physiologic saline solution and exposed to light with an identical time schedule. The animals were killed at the 24th hour,third and seventh day, following light exposure. Cytologic changes in the retinae of both eyes were compared light microscopically. The light exposed left eyes showed mild disorganization of photoreceptor outer segements. Usually this change disappeared by the seventh day. AAA-injected right eyes showed marked destruction in the photoreceptor cell layer. The change in the photoreceptor cells was progressive and disappearance of outer segments and degeneration of numerous nuclei occurred during the following period. （Chin J Ocul Fundus Dis,1992,8:17-19）
【摘要】 目的 探討顱腦損傷(BI)死亡的法醫病理學特點,以及繼發性腦干損傷、并發癥的發生與死亡之間的因果關系。方法 從性別、年齡、致傷方式、損傷類型、生存時間、死亡原因等方面,對四川大學華西法醫學鑒定中心1998年1月-2008年12月127例BI死亡尸檢案例進行回顧性統計研究分析。結果 127例法醫病理學檢案中,原發性BI死亡51例(402%),繼發性腦干損傷死亡61例(480%),并發癥死亡15例(118%),其中傷后12 h內死亡者直接死因均為嚴重原發性腦損傷,存活12 h～1周者直接死因以繼發性腦干損傷居多,生存時間超過1周者約半數死于并發癥。結論 在BI案例的死亡原因確定時,應在全面系統的病理學檢驗基礎上,結合案情及臨床資料進行綜合分析。【Abstract】 Objective To explore the characteristics of forensic pathology in traumatic brain injury and the relationships between secondary brainstem damage, complications and the causes of death. Methods 127 cases were reviewed from gender, age, manner of injury, survival time and the direct causes of death from January 1998 to December 2008. Results Of the 127 cases, the key direct cause of death was secondary brainstem damage, followed by severe primarily brain injury and complications. For those who died within 12 hours after injury, the direct cause was severe primarily brain injury; for those who survived between 12 hours to one week, secondary brainstem damage was in the majority of the causes and for those who survive more than one week time, complication was an important cause. Conclusion In the cases of traumatic brain injury, we should take comprehensive and systematic examination of forensic pathology, and refer to clinical data at the same time to determine the direct cause of death.
Objective To investigate the expression of telomerase reverse transcriptase (TERT) and cell apoptosis in neonatal rats with hypoxia ischemia brain damage (HIBD). Methods A total of 42 7-day-old SD rats (12-18 g, male or female) were randomly allocated into sham-operation group (n=6) and hypoxia-ischemia (HI) group (n=36). In HI group, the rats were anesthetized with ethylether. The right common carotid artery (CCA) was exposed and permanently l igated with a 7-0silk suture through a midl ine cervical incision. A duration of 2.5 hours of hypoxia (8%O2 / 92%N2) was used to produce HIBD model. For sham-operation group, the CCA was exposed without l igation or hypoxia. The brain tissues were harvested at 4, 8, 12, 24, 48, and 72 hours after completion of an HI insult. The expressions of TERT and CC3 were detected by immunohistochemical staining. The apoptosis cells were detected with TUNEL staining method. Results The expression of TERT was increased at 4 hours after HI injury, significantly increased at 24-48 hours and then decreased at 72 hours. The expression of CC3 was increased at 4 hours after HI injury, significantly increased at 24 hours and still maintained high expression at 48 hours and 72 hours. However, in the sham-operation group, both the expressions of TERT and CC3 were extremely low. The expression of TERT and CC3 were higher in the HI group than in the sham-operation group at different time points, and the differences were significant (P lt; 0.05). The TUNEL staining showed that the positive cells in hippocampus and cortical areas were increased at 4 hours after HI injury, significantly increased at 24-48 hours and maintained a high level at 72 hours. However, there was few positive cells in the sham-operation group. There were significant differences between the HI group and the sham-operation group at different time points (P lt; 0.05). Conclusion TERT could be induced by HI in neonatal rats, and might have a protective role in regulating the cell apoptosis in the neonatal HIBD.
Objective Ginsenoside Rg1 could increase the tolerance of neural hypoxia and ischemia under stress, and play an anti-apoptotic effect in hypoxia ischemia brain damage (HIBD). To investigate the effects of ginsenoside Rg1 on neural apoptosis and recovery of neurological function in neonatal rats with HIBD, and to explore the possible mechanism. Methods Fifty-four 10-day-old SD rats (weighing 16-22 g) were randomly allocated into sham-operation group (Sham group, n=6), HIBD model group (HIBD group, n=24), and ginsenoside Rg1 treatment group (Rg1 group, n=24). SDrats in HIBD group and Rg1 group were made the models of HIBD by l igation of the right common carotid artery (CCA) and subsequently hypoxic ventilation (8%O2 plus 92%N2) for 2.5 hours; and in Sham group, the right CCA was only exposed without l igation of CCA and hypoxic ventilation. Intraperitoneal injection of 0.1 mL normal sal ine (NS) containing 40 mg/kg Rg1 was given immediately after operation in Rg1 group, intraperitoneal injection of 0.1 mL pure NS was given in both HIBD group and Sham group and was repeated every 24 hours. The general state of SD rats was monitored after operation, and Longa scores were recorded to evaluate the neurological function at 4, 8, 24, and 72 hours after HIBD. Western blot and immunohistochemistry staining were used to detect protein expressions of both hypoxia inducible factor 1α (HIF-1α) and cleaved caspase 3 (CC3). TUNEL staining was used to evaluate neural apoptosis in situ. Results All rats survived to the end of the experiment. Neurological dysfunction was observed in both HIBD group and Rg1 group, showing significant difference in Longa score when compared with that in Sham group (P lt; 0.05). There was significant difference in Longa score between Rg1 group and HIBD group at 72 hours after HIBD (P lt; 0.05). Western blot showed that the protein expressions of both HIF-1α and CC3 were observed at every time point in every group. The expressions of HIF-1α protein in HIBD group and Rg1 group were significantly higher than those in Sham group at 4, 8, 24, and 72 hours (P lt; 0.05), and the expressions in Rg1 group were significantly higher than those in HIBD group (P lt; 0.05). The expressions of CC3 protein in HIBD group were significantly higher than those in Sham group at 4, 8, 24, and 72 hours (P lt; 0.05), and significant difference was found between Rg1 group and Sham group only at 4 hours (P lt; 0.05). Immunohistochemistry staining demonstrated that HIF-1α and CC3 protein mainly distributed in nucleusand cytoplasma, the results of HIF-1α and CC3 protein expression were similar to the results by Western blot. TUNEL staining showed that the positive cells were characterized by yellow or brown particle confined within nucleus. The number of apoptotic cells at every time point in HIBD group was significantly higher when compared with that in Sham group (P lt; 0.05), and the number of apoptotic cells in Rg1 group was significantly lower when compared with that in HIBD group at 8, 24, and 72 hours (P lt; 0.05). Conclusion Rg1 could inhibit Caspase 3 activation by strengthening and stabil izing HIF-1α signal pathway, and plays a role of anti-apoptosis in neonatal rats with HIBD.
摘要:目的:探討卡配因抑制劑3（MDL28170）對新生大鼠缺氧缺血性腦損傷(HIBD)神經細胞凋亡的影響。方法:建立新生SD大鼠HIBD模型,治療組于缺養缺血后即刻、2 h、4 h腹腔內注射MDL28170,對照組及手術組同時予生理鹽水。缺氧缺血后24 h用免疫組化方法觀察大腦皮質及海馬CA1區Caspase3 蛋白表達、TUNEL法檢測細胞凋亡,觀察組織病理改變并計算海馬神經元死亡數,透射電鏡觀察細胞超微結構。結果:缺氧缺血后24 h缺血側大腦皮質及海馬CA1區Caspase3和TUNEL陽性細胞數較對照組明顯增加,透射電鏡證實有凋亡細胞;MDL28170可減少陽性細胞數量,抑制神經元死亡,差異有顯著性(Plt;0.05)。結論:MDL28170可通過抑制神經凋亡而對新生大鼠HIBD具有一定保護作用。Abstract: Objective: To investigate the effect of (Calpain inhibitor3) MDL28170 on neural apoptosis in a neonatal model of hypoxicischemic brain damage (HIBD). Methods: A neonatal model of HIBD was established, 7dayold SD rats were divided into three groups. The treatment group received MDL28170(ip) at 0 h,2 h,4 h after HI, whereas the other two groups were administered normal saline simultaneously. The expression of caspase3 (by immunohistochemistry), neural apoptosis (by TUNEL) in cortex and hippocampus ipsilateral to the insult were observed 24 h after HI; hippocampal CA1 neural loss and electromicroscopic changes were assessed at the same time. Results: Apoptotic body was observed by electromicroscopy. Caspase3 positive cells and apoptotic cells increased significantly in the ipsilateral cortex and hippocampal CA1 region compared to the control, and MDL28170 reduced the number of positive cells, attenuated CA1 neural loss with significance (Plt;0.05). Conclusion: It is suggested that MDL28170 may protect the brain of neonatal rats after HIBD by suppressing neural apoptosis.