Volume 06 · Issue 02 · 2014

At present, the incidence and growth rate of diabetes is alarming, which is seriously threatening human health^[1]。 Especially in type 1 diabetes, due to the immune dysfunction of the patient, T lymphocytes specifically kill pancreatic islet β cells, which leads to insulin deficiency and diabetes. Millions of people with type 1 diabetes worldwide must be treated with daily insulin injections to stay alive. However, the treatment of insulin can only "treat the symptoms" symptomatically, and long-term high-dose application has potential side effects. Therefore, in clinical practice, how to effectively control T cell-mediated autoimmune response and regenerate pancreatic islet β cells are two key issues to be solved urgently in the treatment of type 1 diabetes. Numerous studies have proved that the autoimmune response of type 1 diabetes has polyclonal properties and multiple immune cell regulation disorders^[2,3]。 All along, in order to overcome type 1 diabetes, countries around the world have explored and clinically tried many treatment options, most of which have ended in failure. Therefore, for a single link, traditional immunotherapy cannot achieve the goal. Some scholars suggest the use of combination therapy for immune intervention, but how and when to combine it is very complicated and will increase the cost of treatment^[1,3]。 In 2012, the International Alliance for Adolescent Diabetes Cure (JDCA) summarized 332 clinical studies, and only 5 technologies (including human islet transplantation, porcine islet transplantation, anti-thymoglobulin (ATG) + granulocyte colony stimulating factor (G-CSF), BCG vaccine and stem cell educator) are likely to cure type 1 diabetes. Among them, the stem cell immune education treatment technology of cord blood pluripotent stem cells (CB-SC) created by us is a brand-new concept for the treatment of type 1 diabetes, which will be introduced in this article.

Type 1 diabetes mellitus (T1DM) is an autoimmune disease. Before the advent of insulin, the time from onset to death of T1DM patients was less than 1 year for children and less than 4 years for adults. The discovery of insulin made T1DM change from a fatal disease to a chronic disease. The American Diabetes Society Diabetes Control and Complications Study (DCCT) shows that intensive insulin therapy can significantly reduce the progression of diabetic retinopathy, neuropathy and nephropathy, but it cannot avoid the continuous decline of pancreatic islet function and eventually the appearance of "fragile diabetes" with drastic fluctuations in blood sugar.

Fulminant Type 1 Diabetes Mellitus (FT1DM) was the disease of 2000 Imagawa et al.^[1]The proposed new subtype of type 1 diabetes mellitus (T1DM) is characterized by hyperacute, complete irreversible destruction of islet β cells, sudden increase in blood glucose, rapid progression of diabetic ketoacidosis, and possible lack of diabetes-related autoantibodies. FT1DM has attracted widespread attention since it was first proposed and has been reported successively in China^[2,3,4,5]。 At present, most reports on FT1DM are concentrated in East Asian populations. Preliminary epidemiological studies have shown that FT1DM accounts for 10% ~20% of patients with T1DM with ketosis or diabetic ketoacidosis^[6]。 Because of the sudden onset, extremely serious metabolic disorders, and can be combined with functional damage of liver, kidney, heart, muscle and other organs, if not diagnosed and treated in time, patients often die in a short time. Therefore, as an acute and critical disease among endocrine and metabolic diseases, FT1DM should be highly valued.

To investigate the prevalence of dyslipidemia and associated risk factors in adult She nationality population in Fujian Province.

Total of 4 838 adults selected from urban and rural areas of Ningde(Tongcheng Subdistrict in Fuding City, Qianqi Town, Shacheng Town), Fujian Province from April 2009 to September 2009 by multi-stage stratified sampling, completed the survey and physical measurements. The height, weight, blood pressure and serum total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol(LDL-C), triglycerides were detected and analyzed by chi-square test and multivariate logistic regression analysis among the different groups.

The overall prevalence of dyslipidemia was 26.6%, the prevalence of dyslipidemia was higher in males than that in females (30.0%(617/2 057) vs 24.0%(667/2 781), χ ²=21.91, P<0.05). The prevalence of high total cholesterol(TC), high LDC-C, low HDL-C and hypertriglyceridemia were 10.1%(488/4 838), 12.6%(609/4 838), 5.2%(252/4 838) and 11.4%(551/4 838), respectively. The prevalence of dyslipidemia increased with age (χ²=30.89, P<0.05) and was associated with sex, body mass index, fasting glucose and blood pressure(OR=0.656, 1.146, 1.059, 1.457, respectively , all P<0.05).

Dyslipidemia is a major public health problem in She population. Steps must be taken to prevent and treat dyslipidemia in She population.

To study the regulatory effects of sterol regulatory element-binding protein-1c (SREBP-1c) on insulin receptor substrate-1 (IRS-1) in rat skeletal muscle cells.

Primary rat skeletal muscle cells were obtained by mixed enzymatic digestion, cells were divided into the following 4 groups: control (C), control+ insulin (C+ I), palmitic acid (PA), palmitic acid+ insulin (PA+ I). L6 myotubes were transfected with adenoviral vectors expressing SREBP-1c with increasing multiplicity of infection (MOI), and divided into groups of green fluorescent protein (GFP), MOI 5, MOI 50, MOI 100 and MOI 200. L6 myotubes were transfected with SREBP-1c siRNA, and divided into groups of control, negative control siRNA, SREBP-1c siRNA.Western blotting and quantitative real-time polymerase chain reaction (RT-PCR) were performed to observe the expressions of SREBP-1c, IRS-1 and protein kinase B (Akt). Cells were stained with Oil Red O to display intracytoplasmic lipid. ANOVA or LSD test were used for data analysis.

Compared with C and C+ I groups, the gene and protein levels of SREBP-1c in PA and PA+ I groups were increased significantly (2.72±0.08 vs 1.00±0.18, 3.02±0.19 vs 1.00±0.05, t=15.240, 18.289, all P<0.05), while the gene and protein expressions of IRS-1 were decreased (0.71±0.04 vs 1.00±0.05, 0.82±0.04 vs 1.00±0.04,t=-7.960, -6.052, all P<0.05), p-IRS-1 (Ser636/639) protein levels were increased, and p-Akt (Ser473) protein levels were decreased (t=20.987, -5.869, all P<0.05). Compared with GFP group, the gene and protein levels of SREBP-1c were increased in a dose-dependent manner in MOI 50, 100 and 200 groups(allP<0.05), while the gene and protein expression of IRS-1 were decreased. P-IRS-1 (Tyr608), and p-Akt (Ser473) protein levels were both decreased significantly in MOI 50 and 100 groups (allP<0.05). Compared with control and negative control siRNA groups, the gene and protein levels of SREBP-1c were decreased in SREBP-1c siRNA group(allP<0.05), while the protein expression of IRS-1 was increased (allP<0.05).

SREBP-1c can inhibit IRS-1 signaling pathway and play an important role in the development of insulin resistance in skeletal muscle cells.

To investigate the effects of amylin on triglyceride metabolism in steatosis human L-02 hepatocyte.

The normal hepatoctyes were incubated with 50% fetal bovine serum high-glucose Duchenne modified Eagle's medium (DMEM) for 72 h to establish the hepatic steatosis model. The experiments were divided into normal hepatocyte cells (Group A), steatosis hepatocyte cells (Group B), steatosis hepatocyte cells incubated with different concentrations of amylin for 24 h (0.01 μmol/L amylin (Group C), 0.1 μmol/L amylin (Group D), 1 μmol/L amylin (Group E) and 5 μmol/L amylin (Group F)). The oil red O staining was used to observe the hepatocyte morphology and intracellular lipid droplets; the hepatocyte triglyceride quantitative detection kit was used to detect the triglyceride levels in each group (mg/g protein); reverse transcription-polymerase chain reaction was used to examine the synthase mRNA and acetyl coenzyme A carboxylase mRNA expression levels in each group. Comparison between the results of the different groups was performed with either one-way analysis of variance (ANOVA ) or Student'st test.

There were lots of red lipid droplets in hepatocyte cells after incubated with 50% fetal bovine serum in high-glucose DMEM medium for 72 h ; the triglyceride levels in group A was (415±52) mg/g protein, and the content was significantly increased in group B with (1129±96) mg/g protein (t=874, P<0.05). After incubated with different concentrations of amylin for 24 h, the triglyceride levels in group C, D, E and F were separately(898±77), (740±83), (515±30) and (628± 48) mg/g protein (F=48.0, P<0.05). The red lipid droplets were reduced by oil Red O staining. Reverse transcription-polymerase chain reaction showed that the intracellular fatty acid synthase mRNA and acetyl coenzyme A carboxylase mRNA expression levels were increased in steatosis hepatocytes and reduced after steatosis hepatocytes incubated with different concentrations of amylin.

When incubated with amylin, triglyceride content in steatosis hepatocytes decreases and the steatosis alleviates and it may be associated with change of the expression levels of fatty acid synthase mRNA and acetyl coenzyme A carboxylase mRNA.

To investigate the effects of insulin glargine (IG) on adipocytokines secretion, lipid synthesis and lipidolysis of human adipocytes in vitro.

Primary preadipocytes were isolated from human subcutaneous adipose tissue and induced to differentiation with different dose of IG(20, 200, 500, 1 000, 1 500 nmol/L). Adipocytokines such as tumor necrosis factor-α (TNF-α), leptin, adiponectin, retinol-binding protein 4 (RBP4) were detected by enzyme-linked immunosorbent assay(ELISA) during the adipogenesis process. Accumulations of intracellular triglyceride (TG) and glycerol released in the medium were used as lipid synthesis and lipolysis index by colorimetric kits.Reverse transcriptase polymerase chain reaction(RT-PCR) was used to observe the effects of IG on adipogenic genes such as PPAR-γ, C/EBPα, adipocytokines gene adiponectin, RBP4, adipocyte fatty acid binding protein(aP2) and lipoprotein lipase(LPL).t-test and AVONA were used to analysis the effects.

(1) Human preadipocytes could be successfully isolated from adipose tissue and induced to mature adipocytes, the secretion of adipocytokines gradually increased with the differentiation. (2) With the differentiation of preadipocytes, TG content gradually increased and reached a peak at 15th days of the differentiation ((12.16±0.19) vs (0.02±0.00) mmol·L^-1·g^-1, t=11.20, P<0.001). Moreover, glycerol content released in the medium was closely associated with IG dose but not associated with the differentiation process, after full differentiation, 1 500 nmol/L group had higher glycerol content than 500 nmol/L group (( 961±15) vs(611±10)μmol/L,t=3.70, P<0.01). (3) RT-PCR analysis showed that gene mRNA expression were increased with the differentiation process and reached the peak at 15th to 21th, days of the differentiation. Compared with undifferentiated cells, they all obviously increased (for PPAR-γ geneP<0.01, other genesP<0.001).

IG can induce the differentiation and secretion of human preadipocytes in vitro, it can also stimulate lipid synthesis in low to moderate concentrations, and induce lipolysis at high concentrations.

To investigate the effect of handle region peptide (HRP) on insulin sensitivity, local renin-angiotensin system and subunits of nicotinamide adenine dinucleotide phosphate(NADPH) oxidase in abdominal adipose tissue in the rats neonatally treated with monosodium L-glutamate (MSG).

The eight-week-old MSG rats were randomly divided into MSG control group (MSG group, n=6), HRP treated group (MSG-HRP group, n=6, 1.0 mg·d^-1·kg^-1 with mini-pump), losartan treated group (MSG-L group, n=6, 450 mg/L in drinking water) and HRP with losartan combined treated group (MSG-HRP-L group, n=6). The period of treatment is four weeks. Normal SD rats (con group, n=6) served as control. At the age of 12 weeks, insulin tolerance test was performed to evaluate the insulin sensitivity. The blood glucose ratio of 30 min to 0 min after infusion of insulin was calculated. The mRNA levels of (Pro)renin, (Pro)renin receptor ((P)RR), angiotensin type 1 receptor (AT1R) and subunits of NADPH oxidase, including P^47phox and P^22phox in abdominal adipose tissue were measured by real-time PCR, and the protein level of angiotensin-Ⅱ (Ang-Ⅱ) was measured by ELISA. ANOVA and LSD-test was performed to estimate difference between groups.

The ratio of blood glucose concentration 30 min after insulin injection to the basic blood glucose concentration was calculated. The MSG group (92%±12%) had the highest level of the ratio and had statistic difference with the Con group (66%±8%), MSG-HRP group (76%±5%), MSG-L group (78%±5%) and MSG-HRP-L group (75%±10%) (F=6.875, all above P<0.05). The (pro)renin mRNA was not detected in abdominal adipose tissue. The MSG-HRP group, MSG-L group, and MSG-HRP-L group had 1.92, 3.19 and 1.90 times (F=9.805, all P<0.05) of (P)RR mRNA expression respectively and had 72%, 45%, and 53% (F=14.508, all P<0.05) of AT1R mRNA expression respectively compared to the MSG group. Compared to the MSG group ((56±4) ng/g protein), local adipose tissue level of Ang-Ⅱ decreased in the MSG-HRP group ((36±8) ng/g protein,P<0.05), and obviously increased in the MSG-L group ((79±14) ng/g protein,P<0.05) and MSG-HRP-L group ((70±16) ng/g protein,F=14.864, all above P<0.05). The MSG-HRP group, MSG-L group and MSG-HRP-L group had 65%, 51% and 43% (F=7.082, all above P<0.05) of P^47phox mRNA expression respectively and had 57%, 40% and 41% (F=9.810, all above P<0.05) of P^22phox mRNA expression respectively compared to the MSG group.

Both of HRP and losartan ameliorated insulin sensitivity with the possible mechanism of decreasing the level of Ang-Ⅱ or inhibiting the effect of Ang-Ⅱ in abdominal adipose tissue, and hence inhibiting oxidative stress.

To investigate the role of human leukocyte antigen (HLA) DQ haplotype for immunoetiologic chassification of idiopathic type 1 diabetes by comparison of clinical features, zinc transporter 8 autoantibodies (ZnT8A), glutamic acid decarboxylase 65(GAD65)-reactive interferon-γ-secreting T cells (GAD65-IFN-γ-T cells).

Fifty-two patients of Han People of Hunan Province origin with newly onset idiopathic type 1 diabetes were enrolled in this study from March 2000 to December 2011. The criteria for enrolment included: new-onset, unprovoked ketosis or ketoacidosis at onset; negative glutamic acid decarboxylase antibody(GADA), protein tyrosinephosphatase antibody (IA-2A) and insulin autoantibody(IAA); permanent insulin deficiency. ZnT8A were detected in all patients with radioligand assay. GAD65-IFN-γ-T cells were tested by enzyme linked immune spot (ELISPOT) in ZnT8A-negative patients. HLA-DQA1 and DQB1 alleles were identified with polymerase chain reaction(PCR) sequence-based genotyping (SBT). According to the situation of HLA-DQ susceptible haplotypes, patients with HLA-DQ genotyping were categorized into two groups, and were all visited annually for 3 consecutive years. Comparisons were made between the two groups in their clinical characteristics, ZnT8A and GAD65-IFN-γ-T cell status. Compare of qualitative data between two groups was progressed by using chi-square test.

In this study group, ZnT8A was positive in 5 cases out of 52 (9.6%), and GAD65-IFN-γ-T cells were positive in 2 cases out of 16 patients with ZnT8A negative (12.5%). More severe diabetic ketoacidosis(DKA)(Z=-2.84, P<0.05) and lower fasting C protein(FCP) levels(χ²=0.38, P<0.05) at onset were observed in patients with HLA-DQ susceptible haplotypes. During the onset, GAD65-IFN-γ-T cells was positive in 1 patient carrying HLA-DQ susceptible haplotypes and there was none in patients with non-susceptible HLA-DQ haplotypes. Islet autoantibodies (ZnT8A and IA-2A) turned positive in 1 patient with HLA-DQ susceptible haplotypes(1/18), while none was observed in patients with non-HLA-DQ susceptible haplotypes during the 3-year visit.

ZnT8A and GAD65-IFN-γ-T cells exist in some patients with idiopathic type 1 diabetes.The patients with idiopathic type 1 diabetes carry HLA-DQ susceptible haplotypes, compared with those without HLA-DQ haplotypes, present a autoimmune tendency.It implies that islet autoimmunity, to some extent, could be an etiology of idiopathic type 1 diabetes, which is probably mediated by HLA-DQ hapalotype.

To analyze the clinical characteristics of adult-onset type 1 diabetic patients (T1DM).

All hospitalized cases of adult-onset T1DM patients in the Department of Endocrinology of Chinese PLA General Hospital from January 1986 to February 2012 were retrospectively analyzed. All the patients were divided into two groups, newly-diagnosed and non-newly-diagnosed group, according to the cut point of 3 months. Newly-diagnosed group were further divided into groups depending on whether the patient was accompanied with ketoacidosis (DKA) or family history of diabetes, and the clinical characteristics were compared between groups. The non-newly-diagnosed patients were divided into 4 groups according to different course of disease: 1-5, 6-10, 11-15 and ≥16 years. Differences in measurement data were compared with least significant difference t test when the data obeyed normal distribution with homogeneity in variance.

Total of 516 cases of adult-onset T1DM patients accounted for 69.5% of all T1DM at the same period, and 133 cases were newly-diagnosed patients, while 383 were not. The average age of onset was (29±8) years. The patients were hospitalized at the age of (37±11) years with a mean body mass index(BMI) of (20.8±3.3) kg/m^2, 19.2%(99/516) of the patients had a family history of diabetes. Fifty-five cases(41.4%) of newly-diagnosed patients were associated with DKA and 29 cases (21.8%) had a family history of diabetes; fasting blood glucose and blood uric acid in patients associated with DKA was significantly higher than those in patients without DKA(t=4.019, 2.288, both P<0.05). Seventy cases(18.3%) of non-newly-diagnosed patients had a family history of diabetes. In the non-newly-diagnosed group, compared with those in the patients without family history of diabetes, the triglyceride level(t=1.263, P<0.05) was higher and incidence of hypertension, chronic renal failure and non-proliferative diabetic retinopathy were higher in patients with a family history(χ²=16.029, 5.843, 10.164, all P<0.05); and high blood pressure also occurred earlier in patients with a family history(t=2.769, P<0.05). The BMI, uric acid, total cholesterol, glycated hemoglobin A1c was different significantly in patients with different duration of disease(H=29.282, 16.590, 12.530, 50.590, all P<0.05). The incidence of clinical nephropathy, chronic renal insufficiency, retinopathy and autonomic neuropathy reached apex in patients with disease duration of 11-15 years.

Adult-onset T1DM has unique clinical features, and its chronic complications and the incidence of complications related with family history of diabetes, the incidence of microvascular complications reaches peak in patients with disease duration of 11-15 years.

To investigate the effects of liraglutide on cognitive function in patients with type 2 diabetes mellitus and the underlying Mechanism.

The cognitive function of type 2 diabetics treated in our hospital from November 2012 to May 2013 was evaluated with Montreal Cognitive Assessment(MoCA score). Subjects with cognitive dysfunction were screened out and divided into liraglutide group (LI group) or non-liraglutide group(NLI group). Patients in LI group were received liraglutide for 12 weeks. Patients in NLI group were given non- liraglutide drugs(such as insulin, metformin, acarbose, sulfonylureas, etc) for 12 weeks. The levels of serum Aβ, fasting plasma glucose, glycosylated hemoglobin, blood lipids, body weight were measured, and the cognitive function was evaluated again. The χ² test or t text and the multiple factor correlation analysis were used for statistical analysis.

In LI group, the cognitive function was improved in 44.2% (19/43) of patients. The overall MoCA score of (23.0±1.9) points rised up to (25.1±2.0) points. There were 19 cases in LI group whose post-treatment score reached (27.0±0.8) points. The difference was statistically significant(t=8.975, P<0.05). Only 2.6% (1/39) of patients in NLI group had better cognitive function, and the overall MoCA score was (23.2±1.7) points before treatment, while (23.2±1.5) points after treatment(t=0.09, P>0.05). In LI group, Serum Aβ levels reduced from (266±98) ng/L to (256±96) ng/L, the body weight reduced from (83±12) kg to (80±11) kg. The difference was statistically significant(t=-2.76, -2.89, all P<0.01). While Aβ levels increased and body weight did not change significantly in NLI group. Correlation analysis showed that the improved cognitive function was relevant to the application of liraglutide (r=0.57, P<0.05), weight loss (r=-0.42, P<0.05) and Aβ decrease (r=-0.28, P<0.05) .

Liraglutide could improve the cognitive ability of type 2 diabetes patients and its mechanism might be relevant to the reduction of serum Aβ level and body weight.

To estimate health economic effect of community fore-warning and health management system construction among high-risk diabetes persons in Tianjin.

We collected information of general cost of the program investment, the intervention cost and the actual effect of the blood glucose outcome for each participant, and estimated health cost effect. Three hundred and seven individuals with high risk of diabetes were enrolled to manage health. Cost-effect ratio, general cost and the intervention cost of each indicidual were calculated. We used above result and references data to estimate the health economic effect and cost-effect ratio for developing health management of the community diabetes high-risk population in the whole Tianjin. Paired t test and matched χ² test were used to analyze continuous variables and classified variables, respectively.

The intervention cost for every participant was RMB 628 yuan. The intervention reduced the incidence of diabetes by 52.5%. The cost-effect ratio was 1∶4.66.

The economic effect of preventing or delaying type 2 diabetes by lifestyle intervention is very remarkable.

Glutamate decarboxylase (GAD) belongs to endocrine enzymes, including two isoenzymes, GAD65 and GAD67, but only GAD65 is an important islet autoantigen. Numerous studies have identified GADA as the most sensitive and widely used indicator for diagnosing and predicting type 1 diabetes mellitus (T1DM) and adult occult autoimmune diabetes mellitus (LADA^[1,2]。 There are various methods for GADA detection, including radioligand assay and enzyme-linked immunosorbent assay (ELISA), but the diagnostic sensitivity and specificity are closely related to the purity and antigenicity of GAD65 protein. However, antigen-specific T cells can directly reflect the autoimmune status of pancreatic islets, which can improve the efficiency of antibody diagnosis of T1DM. Studies have shown the use of tyrosine phosphatase (IA-2), GAD65, islet cell-specific glucose-6-phosphatase catalytic subunit-associated protein (IGRP), and proproinsulin as CD8 in newly diagnosed T1DM patients^＋The diagnostic sensitivity of T cell stimulating antigen varies from 25% to 40%, and the specificity varies from 87% to 100%^[3]。 Subsequent T-cell assay International Standardization Working Group confirmed that GAD_270-285It is the main stimulating fragment of human leukocyte antigen (HLA) class II molecular tetramer detection technology^[4,5]。 Therefore, the selection of an appropriate GAD65 antigen or protein fragment can improve the diagnostic sensitivity and specificity of GADA or autoreactive T cells.

Although genes and lifestyle are widely believed to be the main factors in increased risk of diabetes, genetic alterations can only partially explain the increased risk of diabetes. Early developmental environment (nutritional status) can significantly affect the risk of developing diabetes in adulthood. Epigenetics is closely related to the pathogenesis of chronic diseases such as diabetes, metabolic syndrome and cancer. Because epigenetics can be stimulated by the environment and change, and the altered epigenetic characteristics can be maintained and existed in cell division, epigenetics is probably an important molecular basis for the abnormality of early developmental environment and the disorder of glucose metabolism in adulthood. In addition, more and more animal models and large-scale clinical research data show that epigenetic mechanisms play a key role in the development of glucose metabolism abnormalities in adulthood^[1]。 This article will briefly introduce it as follows.

Beverages refer to liquid foods that are produced by different formulas and manufacturing processes using water as the basic raw material for people to drink directly. There are many kinds of beverages, including carbonated beverages, fruit and vegetable juice beverages, milk-containing beverages, functional beverages, tea beverages, etc. Beverages such as sugars (sucrose, glucose, fructose) are called sugary beverages. In 2008, the Ministry of Health issued the Administrative Code for Food Nutrition Labeling, which stated that sugars in beverages provide 4 kcal of energy per gram^[1]。 Today, as people start to consciously control the intake of high-fat and high-sugar solid foods aimed at obesity, the negative impact of increased energy intake brought by sugary drinks on body weight is gradually attracting attention. This paper makes a literature review on the related research progress.

Infection is the most common comorbidity in diabetic patients. Furuncle is more common in soft tissue infection of scalp, while abscess perforating folliculitis of scalp is rare. Abscessful perforating perifolliculitis of the scalp (PCAS) is a rare chronic inflammation with unknown etiology, usually characterized by suppurative folliculitis of the scalp, painful nodules, sinus formation, cicatricial alopecia, etc. Its etiology and pathogenesis are unknown, mostly related to immune factors and secondary infection, and clinical treatment is difficult^[1]。 A case of type 2 diabetes with this disease as the first onset admitted to our hospital is reported as follows.

Diabetic peripheral neuropathy (DPS) is one of the most common chronic microvascular complications of diabetes mellitus. It is divided into five subtypes according to different clinical manifestations. Among them, distal symmetric polyneuropathy (DSPN) is the most common subtype causing neuropathic pain in patients. According to statistics, 15% ~20% of diabetic patients suffer from painful DSPN. The risk of foot ulcer and Charcot neuropathy in patients with painful DSPN and the mortality rate of patients are significantly increased, which seriously affects the quality of life of patients. Therefore, the screening and prevention of painful DSPN should be strengthened, and the patients who have already developed painful DSPN should be actively treated.

Infection is the main causative factor of diabetic foot syndrome, which is aggravated by infection with multidrug-resistant bacteria such as methicillin-resistant Staphylococcus aureus (MRSA). Severe MRSA infection requires aggressive treatment and close monitoring of the recovery process to obtain the best clinical endpoint.

Educating people with diabetes can change their behavioral habits, which may help prevent diabetic foot ulcers and amputations. However, there are currently few reports on factors associated with improving the effectiveness of foot care education. This study involved 100 patients with type 2 diabetes, including 52 diabetic patients with diabetic foot syndrome and 48 patients with ischemic disease of the lower extremities. The study used a structured assessment system based on practical reasoning protocols to collect data from patients before education. Then, oral and written education were adopted to carry out nursing education of diabetic foot. After education (6 months), the data were obtained by questionnaire survey. The obtained data are then analyzed using content analysis, descriptive statistics and inferential statistics.

The patient's reduced pain threshold after and after trauma is one of the main features of diabetic neuropathy. Pain sensing nerve endings (A-delta fibers and C fibers) continue to deteriorate as receptors of nociceptive stimuli, resulting in a decrease in the patient's ability to regulate sharp pain (first pain) by A-delta fibers and dull pain (second pain) by C fibers. However, patients with diabetic neuropathy and acute Shake's foot often have deep dull pain when walking, so it is necessary to establish a canonical pain hypothesis in acute Shake's foot.