Biochemistry is one of the important basic courses for medical speciality.This article discussed the four aspects of how to improve the quality of biochemistry instruction,such as strengthening young teachers'sense of responsibility in teaching,and building up their professional knowledge training and so on.To young teachers,this paper may be useful for improving the quality of medical biochemistry teaching.

Objective:This study aimed to investigate the role of mitochondrial fusion protein 2 (Mfn2) in chronic renal injury caused by cyclosporine A (CSA) and the possible mechanism.Methods:The model of chronic CSA nephropathy was established in rats. The rats were divided into solvent control group, CSA model group and normal control group. Serum creatinine and urinary protein levels were detected. The tubulointerstitial injury was observed by light microscopy. The changes of mitochondrial structure were observed by electron microscope, and the expression of Mfn2 was detected by Western blot.Results:The levels of serum creatinine and urinary protein in CSA model group at 2 and 4 weeks were significantly higher than those in control group and solvent group ( P<0.05). In CSA model group, tubulointerstitial injury was obvious, mitochondria swelling and deformation were found in tubular epithelial cells, and ridge disappeared. Compared with normal control group and solvent control group, the expression of Mfn2 in CSA model group was significantly decreased at 2 and 4 weeks ( P<0.05), and the expression of Mfn2 in CSA model group at 4 weeks was further decreased compared with 2 weeks ( P<0.05). Conclusions:Mfn2 may play an important role in the injury of tubular epithelial cells caused by cyclosporine.

Climacteric ; Depression ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Middle Aged ; Phytotherapy ; Sleep Initiation and Maintenance Disorders ; Syndrome

Disorders of sex development(DSD) include anomalies of sex chromosomes,gonads,reproductive ducts,and genitalia.Here,the term "intersex" is avoided because of its imprecision.The purpose of this review is to assist health care professionals in the provision of treatment,education,and support to children born with DSD and to their families.The goal of DSD treatment is to achieve the long-term physical,psychological,and sexual well-being of the patients.In the case of DSD it involves several principles.Providing medical and surgical care to deal with a complication that threatens to the patient's physical well-being;minimizing the potential for the patient and family to feel ashamed,stigmatized,or overly obsessed with genital appearance;delaying elective surgical and hormonal treatments until the patient can actively participate in decision-making;telling the truth to the family and the child and addressing psychosocial distress of the children and their parents.This approach is termed as "patient-centered".

BACKGROUND: Because the continuity and integrity of the trachea are likely damaged to some extent after tracheostomy, the implementation of sequential ventilation has certain difficulties, and sequential invasive-noninvasive ventilation on patients after tracheostomy is less common in practice. The present study aimed to investigate the feasibility of invasive-noninvasive sequential weaning strategy in patients after tracheostomy. METHODS: Fifty patients including 24 patients with withdrawal of mechanical ventilation (conventional group) and 26 patients with sequential invasive-noninvasive weaning by directly plugging of tracheostomy (sequential group) were analyzed retrospectively after appearance of pulmonary infection control (PIC) window. The analysis of arterial blood gases, ventilator-associated pneumonia (VAP) incidence, the total duration of mechanical ventilation, the success rate of weaning and total cost of hospitalization were compared between the two groups. RESULTS: Arterial blood gas analysis showed that the sequential weaning group was better than the conventional weaning group 1 and 24 hours after invasive ventilation. The VAP incidence was lowered, the duration of mechanical ventilation shortened, the success rate of weaning increased, and the total cost of hospitalization decreased. CONCLUSION: Sequential invasive-noninvasive ventilator weaning is feasible in patients after tracheostomy.

Adult ; Aged ; Aged, 80 and over ; DNA Primers ; Female ; Humans ; Lymphoma ; genetics ; Male ; Middle Aged ; Mutation ; Myeloid Differentiation Factor 88 ; genetics ; Polymerase Chain Reaction

ObjectiveThe purpose of this study was to evaluate the effect of prostaglandin E1 (PGE1) on blocking the development of acute respiratory distress syndrome (ARDS) induced by acid aspiration. MethodsTwenty new Zealand rabbits were used. Dilute HCl was instilled into right bronchus of the rabbits. The rabbits were then divided randomly into two groups: injury group and treatment group. In injury group ( n = 10) rabbits received no treatment except mechanical ventilation. In treatment group ( n = 10) immediately after acid instillation the rabbits received an intravenous bolus of PGE1 followed by a continuous infusion. Blood gas, airway pressure and dynamic and static compliance were measured before and after acid instillation. Blood samples were taken from artery for determination of 6-k-PGF1α, TXB2, NO2-/NO3- and ET-1. The animals were killed and the wet/dry lung weight (W/D) ratio and total protein of bronchoalveolar lavage fluid(BALF) of right lung were measured. Microscopic examination of the lung was done. ResultsIn treatment group PaO2 was significantly higher than that in injury group after acid instillation. Plasma 6-k-PGF1α and NO2-/NO3- levels were significantly higher in treatment group while plasma TXB2 and ET-1 levels were significantly lower. W/D ratio and TP of BALF of right lung were significantly lower in treatment group. The inflammatory changes were diffuse in injury group while in treatment group they were localized and less severe. Conclusions PGE1 can lessen severity of ARDS induced by acid aspiration. It may protect pulmonary vascular endothelial cells through maintaining the balance between PGI2 and TXA2 and that between NO and ET-1 .

Objective To study the role the pathogenesis of early acute lung injury (ALI) of rabbits induced by intravascular injection of endotoxin (ET) with the intervening method of Chloroquine. Methods Rabbits were randomly assigned to three groups: control group, ET group, and ET+ chloroquine group. Acute lung injury was induced by intravascular injection of ET (500μg/kg). The arterial gas analyses, leucocyte and platelet counts in peripheral blood, PLA2 activity both in serum and lung tissue, lipid peroxide (LPO) and superoxide dismutase (SOD) in lung tissue were measured. Electron microscope and light microscope were used to observe the pathological injuries in pulmonary tissue. The protective effects of chloroquine in early ALI were evaluated. Results Compared with saline controls, rabbits treated with ET displayed the early lung injuries, such as the decrease of PaO2 (P＜0.05), the decrease of leucocytes and platelets in peripheral blood, the leukocytes sequestration in lung tissue. The PLA2 activity significantly increased in ET group compared with control group and chloroquine group both in serum and pulmonary tissue. In ET group, concentration of LPO increased in lung tissue (P＜0.05), while concentration of SOD decreased (P＜0.05). Severe histopathological injuries were presented in ET group, including pulmonary edema, lung tissue haemorrhage, inflammatory cells infiltration, asphyxial membrand formation, partial pulmonary closure and emphysema.Ultrastructural changes showed both type Ⅰ and type Ⅱ epithelial cells injury in ET group, the edema of endothelial cells, interalveolar septum thickening. In chloroquine group, PaO2 didn't decrease, PLA2 activities in serum and pulmonary tissue were lower than ET group (P＜0.05, P＜0.05), while the concentration of LPO in lung tissue decreased (P＜0.01) and SOD increased significantly (P＜0.01). Pathological examination showed slight pulmonary edema, inflammatory cells infiltration were extenuated, ultrastructural examination proved that the injuries were alleviated by chloroquine compared with ET group. Conclusion Intravascular injection of ET could successfully induce the early ALI models in rabbits. Chloroquine could inhibit the PLA2 activation and reduce the oxidative injury in lung tissue. The experiment result demonstrated PLA2 activation and oxidative stress played important roles in the pathophysiological process of early ET-induced ALI in rabbits.

Objective To study the changes in activity of phospholipase A2 (PLA2) in the course of endotoxin (ET) induced acute lung injury (ALI) inrabbits and the antagonizing effect of fructose-1, 6-diphosphate (FDP), in order to evaluate the therapeutic effect of FDP on ET-induced ALI. Methods Flapeared white rabbits were randomly assigned to three groups: control group (group A), ET challenge group (group B) and treatment group (ET challenged followedby FDP, group C). Group A animals were injected with saline (2ml/kg) as control. Group B animals were injected with ET (500μg/kg) solution followed by saline. Total amount of liquid was 2ml/kg. Group C animals were given the same amount of ET solution followed by injection of FDP (300mg/kg) solution. Total amount of liquid was also 2 ml/kg. During the experiment, respiratory rate, heart rate, blood pressure, arterial blood gases and the plasma PLA2 activity were determined at 0h, 0. 5h, 2h, 4h and 6h respectively. The rabbits were sacrificed at 6h, pulmonary PLA2 activity was assessed, and the pathologic changes in pulmonary tissues were examined with light microscope and transmission electron microscope. Results Compared with group A,rabbits of group B manifested the typical characters of ALI after ET injection, and the PLA2 activity in both serum and pulmonary tissue was much higher than those of group A (P＜0. 01).Values of the PLA2 activity in group C were between those of the two former groups. At the rame time, obvious pathological changes indicating lung injury were observed in group B and only mild pathological changes could be discerned in group C. Conclusion Activation of PLA2 activity is an important factor in pathogenesis of ET-induced ALI. FDP can antagonize the PLA2 activity and protect rabbits from early ET induced ALI to a certain extent.

Objective To investigate the effects of nitric oxide (NO) inhalation on the expression of TNF-?,IL-8 and CD11b mRNA in lung tissue during acute respiratory distress syndrome (ARDS) induced by intravenous injection of endotoxin in dogs.Methods Twelve pure bred beagle dogs of both sexs weighing 8-12.5 kg were randomly divided into 2 groups: NO group received mechanical ventilation with NO inhalation (n = 6) and control group received only mechanical ventilation ( n = 6) . Sepsis and ARDS were induced by intravenous injection of endotoxin as described in detail in our previous paper. Hemodynamics and pulmonary oxygenation were monitored and shunt fraction was calculated. At the end of experiment the animals were sacrificed and lung tissue was obtained aseptically and stored in the liquid nitrogen at - 180℃ . The total RNA was extracted. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of TNF-?,IL-8 and CD11b mRNA. The total RNA was reversely transcripted to cDNA. Then the cDNA was amplified by PCR. The product of PCR was scanned by gel-image analysis system.?-action was used as internal control. Semi-quantitative method was adopted for measurement of TNF-? ,IL-8 and CD11b mRNA expression. Results The expression of TNF-?, IL-8 and CD11b mRNA in lung tissue was significantly decreased in NO group compared with those in control group.Conclusion NO inhalation reduces expression of TNF-?, IL-8 and CDllb mRNA in lung tissue during ARDS induced by intravenous endotoxin.