Objective: To observe the survivability of Lactobacillus acidophilus in short peptide enteral nutrition liquid.Methods: 5% fermentative medium of Lactobacillus acidophilus was added in 12% short peptide enteral nutrition liquid.The preparations were cultured at 37℃ anaerobic condition.Samples were taken from culture at 0,4,8,12,14,16,20,24 h during fermention.The living bacteria counts,A_600,acidity and pH values were examined respectively.Results: The number of Lactobacillus acidophilus increased at 0 to 16 h.A_600 ascended during the time.Acidity ascended with time.Conclusion: The present study demonstrated that Lactobacillus acidophilus had better survivability in 12% short peptide enteral nutrition liquid,and the terminal time should be controlled during 12~14h.

Objective The invasion and metastasis of tumor cells depend on the growth of new blood vessels, and tumor neovascularization was regulated by a lots of factors. This study aimed to investigate the expression of hypoxia-inducible factor-1α (HIF -1α) and vascular endothelial growth factor (VECF) in retinoblastoma and explore the correlation of HIF-1α and VEGF with tumor invasion and metastasis and analyze their relationship with clinicopathology characters and determine their effect on angiogenesis. Methods Forty-six retinoblastoma specimens with different clinical stages were collected in Affiliated Second Hospital of Nanchang University. The specimens received neither radiotherapy nor chemotherapy. The retinal tissue near the tumor was as control. Immunohistochemistry was used to detect the expression of HIF-1α protein and VEGF protein in retinoblastoma. The relationship between expression of HIF-1α and VEGF and stage of tumor was analyzed. Results The HIF-1α and VEGF were highly expressed in the ischemia or necrosis area of retinoblastoma. Expression of HIF-1α was mainly in cell nuclear and partly in cytoplasm, and VEGF was mainly expressed in cytoplasm of tumor cells. The expression of HIF-1α and VEGF was gradually increased with the rising of tumor stage (P ＜ 0. 05) and showed significant correlation between expression of HIF-1α and VEGF with tumor stage(r_s =0. 943, P ＜0. 01). HIF-1α exepression was also possitively related to VEGF level in retinoblastoma (r, =0. 946, P ＜ 0. 01). Conclusion HIF-1α and VEGF were over-expressed in retinoblastoma cells, and the expressions were related to clinical staging, invasion and metastasis of tumor cells. The expression of HIF-1α and VEGF was one of the predictors for the biological behaviors of retinoblastoma. HIF-1α and VEGF may play an important role in angiogenesis and tumor progression in retinoblastoma.

OBJECTIVETo investigate the relative effects of degree and distribution of body fat with several cardiovascular disease (CVD) risk factors in elderly Chinese subjects.

METHODSOne hundred and thirty-five elderly Chinese individuals (age range, 60-65 y) without any history of significant renal, hepatic or cardiac disease were recruited. Seated blood pressure, anthropometric and fasting plasma biochemical parameters were measured. Student's t-test was used to compare the differences in biochemical and anthropometric markers between cohorts.

RESULTSMales were heavier (64.6 +/- 8.6, 57.2 +/- 8.2kg, P < 0.001), taller (1.65 +/- 0.06, 1.51 +/- 0.05 m, P < 0.001) and their greater body fat was predominantly deposited centrally (Waist-to- hip ratio, 0.91 +/- 0.06, 0.88 +/- 0.07, P < 0.05). Females were more generally obese with increased body mass index (BMI, 23.8 +/- 4.6, 25.0 +/- 3.5 kg/m2, P < 0.05) and percentage body fat [26.3% (24.5%-28.1%) vs 37.2% (36.0%-38.9%), P < 0.001] than the males. However, despite an 11% higher proportion of body fat in females, no significant differences were identified in blood pressure, lipid profile, indices of insulin resistance or albumin-to-creatinine ratios.

CONCLUSIONIt is likely that central adiposity contributes disproportionately to these metabolic disorders in males even though they are much leaner than elderly Chinese females.

Adult ; Aged ; Body Mass Index ; Cardiovascular Diseases ; etiology ; Female ; Humans ; Male ; Middle Aged ; Obesity ; complications ; Risk Factors

PURPOSETo review evidence-based management of nephropathy in patients with type 2 diabetes.

DATA SOURCESA literature search (MEDLINE 1966 to 2000) was performed using the key word "diabetic nephropathy". Relevant book chapters were also reviewed.

STUDY SELECTIONWell-controlled, prospective landmark studies and expert review articles on diabetic nephropathy were selected.

DATA EXTRACTIONData and conclusions from the selected articles that provide solid evidence to the optimal management of diabetic nephropathy were extracted and interpreted in light of our clinical research experience with many thousands of Hong Kong Chinese patients.

RESULTSHypertension, long diabetes duration, poor glycaemic control and central obesity are the most important risk factors. Microalbuminuria is a practical marker to predict overt nephropathy in type 2 diabetic patients. Risk factor modification, renal function monitoring and combined therapies are the current integrated approaches to manage patients with diabetic kidney disease. Optimal glycaemic control is the mainstay of treatment but effective antihypertensive therapy is also key to delaying the progression of diabetic nephropathy. Angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists have important renoprotective actions independent of their blood pressure lowering actions.

CONCLUSIONSDiabetic nephropathy is the leading cause of end-stage renal disease worldwide. Monitoring renal function and screening for microalbuminuria will allow the identification of patients with nephropathy at a very early stage for intervention. Tight glycaemic control and aggressive antihypertensive treatment as well as the use of renin-angiotensin system inhibitors should substantially delay the progression of nephropathy.

Albuminuria ; diagnosis ; therapy ; Blood Glucose ; analysis ; Diabetes Mellitus, Type 2 ; complications ; Diabetic Nephropathies ; epidemiology ; therapy ; Dietary Proteins ; administration & dosage ; Humans ; Hyperlipidemias ; therapy ; Hypertension ; therapy

Acute kidney injury is a clinical syndrome that can be caused by numerous diseases including acute tubular necrosis (ATN). ATN evolves in several phases, all of which are accompanied by different immune mechanisms as an integral component of the disease process. In the early injury phase, regulated necrosis, damage-associated molecular patterns, danger sensing, and neutrophil-driven sterile inflammation enhance each other and contribute to the crescendo of necroinflammation and tissue injury. In the late injury phase, renal dysfunction becomes clinically apparent, and M1 macrophage-driven sterile inflammation contributes to ongoing necroinflammation and renal dysfunction. In the recovery phase, M2-macrophages and anti-inflammatory mediators counteract the inflammatory process, and compensatory remnant nephron and cell hypertrophy promote an early functional recovery of renal function, while some tubules are still badly injured and necrotic material is removed by phagocytes. The resolution of inflammation is required to promote the intrinsic regenerative capacity of tubules to replace at least some of the necrotic cells. Several immune mechanisms support this wound-healing-like re-epithelialization process. Similar to wound healing, this response is associated with mesenchymal healing, with a profound immune cell contribution in terms of collagen production and secretion of profibrotic mediators. These and numerous other factors determine whether, in the chronic phase, persistent loss of nephrons and hyperfunction of remnant nephrons will result in stable renal function or progress to decline of renal function such as progressive chronic kidney disease.
Acute Kidney Injury ; Collagen ; Extracellular Traps ; Hypertrophy ; Inflammation ; Necrosis* ; Nephrons ; Phagocytes ; Re-Epithelialization ; Renal Insufficiency, Chronic ; Wound Healing

RNA viruses are critically dependent upon virally encoded proteases to cleave the viral polyproteins into functional proteins. Many of these proteases exhibit a similar fold and contain an essential catalytic cysteine, offering the opportunity to inhibit these enzymes with electrophilic small molecules. Here we describe the successful application of quantitative irreversible tethering (qIT) to identify acrylamide fragments that target the active site cysteine of the 3C protease (3C^pro) of Enterovirus 71, the causative agent of hand, foot and mouth disease in humans, altering the substrate binding region. Further, we re-purpose these hits towards the main protease (M^pro) of SARS-CoV-2 which shares the 3C-like fold and a similar active site. The hit fragments covalently link to the catalytic cysteine of M^pro to inhibit its activity. We demonstrate that targeting the active site cysteine of M^pro can have profound allosteric effects, distorting secondary structures to disrupt the active dimeric unit.