ObjectiveTo systematically review the associations of maternal diabetes mellitus with cleft lip and palate in offspring. MethodsThe PubMed, Embase, Cochrane Library, Web of Science, CNKI, VIP and WanFang Data databases were electronically searched to collect the observational studies on the association of maternal diabetes mellitus with cleft lip and palate in offspring from inception to June 30, 2024. Two reviewers independently screened literature, extracted data and assessed the risk of bias of the included studies. Meta-analysis was then performed by using Stata 17.0 and RevMan 5.4 software. ResultsA total of 34 studies involving 2 556 911 participants were included. The results of meta-analysis showed that maternal pregestational diabetes mellitus was associated with an increased risk of cleft lip and palate in offspring (OR=1.91, 95%CI 1.59 to 2.30, P<0.01). Maternal type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) were also associated with an increased risk of cleft lip and palate in offspring (T1DM: OR=2.28, 95%CI 1.65 to 2.30, P<0.01; T2DM: OR=1.87, 95%CI 1.10 to 3.19, P<0.01). There was no correlation between maternal gestational diabetes mellitus and cleft lip and palate in offspring. ConclusionCurrent evidence shows that maternal pregestational diabetes mellitus was associated with an increased incidence of cleft lip and palate in offspring. Due to the limited quality and quantity of the included studies, more high quality studies are needed to verify the above conclusion.
Objective
To analyze the expression of apoptosis-related genes of retinal blood vessel in early diabetic rats by gene chip technology.
Methods
To make diabetic rat model by intraperitoneal injection of streptozotocin (STZ). On the 6th week after blood pressure increased, 10 rats were executed in Diabetic group and normal control group respectively. 20 retinal blood vessels were extracted and the RNA was isolated. The probe was made of alpha;-32 P-deoxyadenosine triphosphate (dATP)-labeled sample which hybridized 1176 nylon chips, and then analyzed by software. Three different expression genes were selected to verify by reverse transcription polymerase chain reaction (RT-PCR).
Results
On the 6th week, 136 （11.5％） genes were differentially expressed ［up-regulated genes were 90(7.6%), down-regulated genes were 46(3.9%)］in diabetic group. These genes involved into different groups according to their function. Especially in 72 apoptosis-related genes, 15 genes were differentially expressed. The up-regulated genes were some TNF receptor family members such as TNFRSF12, TRAIL, TNFRSF9, FADD；Bcl-2 family members such as bcl-w, bax, bak1 and AKT. The down-regulated genes were FAF1 which related to fas.
Conclusions
The expression of retinal vascular gene in early diabetic rats has been changed complicatedly. In particular, the multiple apoptosis-related genes have been changed in early diabetic, and most of them are at the upstream of apoptosis pathway. These findings indicate that the development of diabetic retinopathy is associated with multiple signaling pathways leading to apoptosis, while the alterations on the level of molecular biochemistry are still limited in apoptosis induction period.
（Chin J Ocul Fundus Dis，2008，24：244-248）
Objective To observe the effect of diabetic retinopathy on endothelial progenitor cells (EPCs) from peripheral blood. Methods Sixty male Wistar rats were divided into control group and diabetes group. The rats in diabetes group were induced with streptozotocin (STZ) injection for diabetic retinopathy model. Flow cytometry was used to identify and count the number of EPCs from peripheral blood at 1 week, 1, 3 and 6 months after injection. All eyeballs were examined by hematoxylin and eosin (HE) staining, periodic acidSchiff's (PAS) staining of trypsin-digested retinal vessels flat preparation and transmission electron microscope. EPCs count, and the relationship between DR morphological changes and EPCs count were compared and analyzed. Results The quantity of EPCs from peripheral blood at 1 week, 1, 3 and 6 months after STZ injection were 25plusmn;7, 28plusmn;8, 39plusmn;7, 43plusmn;7 cells per 200 000 monocytes respectively, which decreased compared with the control group 45plusmn;4 cells per 200 000 monocytes (F=8.933，Plt;0.01). The quantity of EPCs was gradually increased at 1 week, 1, 3 and 6 months after STZ injection, accompanied with responsive pathological changes of retinal structure and vessels. The thickness of retina at 1 week and 1 month after injection were reduced slightly. The number of retinal ganglion cells reduced, with the time passing by. Endothelial cells were edema, mitochondrial was swollen, capillary basement membrane was thicken, lumen was significant stenosis, lumen occlusion and retinal artery aneurysm were observed at 6 months after STZ injection. Conclusion The number of EPCs increases gradually throughout the development of DR.
Objective To observe the abnormal expression of alpha;A-crystallin protein in neural retina in type 2 diabetic rats via proteomic technique.Methods Twenty-eight male Sprague-Dawley (SD) rats were randomly divided into the normal control and the diabetic experimental groups with 14 rats in each group.A type 2 diabetes rat model (T2DM) was set up in the diabetic experimental group by feeding high fat diet combined with peritoneal injection of low dose streptozotocin (STZ);the successful diabetes model is with the randomlydetected blood glucose of ＞16.7 mmol/L.The rats in the control group underwent peritoneal injection of equivalent sodium citrate solution and were fed with normal diet.All of the animals were sacrificed by decapitation 56 days after the induction of diabetes.The eyes were enucleated and the neural retina layers were carefully peeled off and preserved.The total neural retinal proteins were extracted from the control and diabetic groups, respectively,and then subjected to two dimensional gel electrophoresis (2-DE).Some different proteins spots were identified by peptide mass fingerprinting (PMF) as well as by tandem mass spectrometric (MS/MS) measurements.Western blot and indirect immunofluorescence (IMF) were used to confirmed that alpha;A-crystallin protein expression was upregulated in diabetic retina.Results An average of （3122plusmn;37） spots in normal retinas and（2702plusmn;21）spots in diabetic group were found by 2-DE image analysis software; about 150 spots in 2-DE gel of diabetic retinae exhibited statistically significant variations (t＞2.77,P＜0.05).Compared with normal rats' retinae, diabetic ones presented 68 protein spots of up regulation expression and 82 of downregulation expression in 2DE gel.Furthermore,20 of the 150 protein spots were identified by mass spectrometry.The points of 2369 and 1048 in 2-DE gel, showing high expression in diabetic retinal tissues, were identified as alpha;A-crystallin via PMF.Western blot validated that the expression level of alpha;A-crystallin in diabetic neural retina was much higher than that in the control group. Significantly increased expression of alpha;A-crystallin in nuclear retina in diabetic group was also observed by IMF. Fluorescence was mainly seen in the retinal nuclear layer;alpha;A-crystallin aggregation was detected in the perinuclear region of neurons.Conclusion The expression of alpha;A-crystallin increases in neural retina of early T2DM rats.
ObjectiveTo systematically review the clinical efficacy and safety of hyperbaric oxygen therapy as adjunctive treatment for diabetic foot ulcers.
MethodsSuch databases as The Cochrane Library (Issue 1, 2014), PubMed, EMbase, CBM, VIP, CNKI and WanFang Data were searched up to January 2014 for randomized controlled trials (RCTs) about hyperbaric oxygen therapy as adjunctive treatment for diabetic foot ulcers. According to the inclusion and exclusion criteria, two reviewers independently screened literature, extracted data, and assessed methodological quality of included studies. Then, meta-analysis was performed using RevMan 5.2 software.
ResultsFourteen RCTs involving 910 patients were included. The results of meta-analysis showed that, hyperbaric oxygen therapy combined with routine therapy was superior to routine therapy alone regarding ulcer healing rates (RR=2.16, 95%CI 1.43 to 3.26, P=0.000 3), incidence of major amputation (RR=0.20, 95%CI 0.10 to 0.38, P < 0.000 01), reduction of ulcer area (MD=1.73, 95%CI 1.34 to 2.11, P < 0.000 01), and improvement of transcutaneous oxygen tension (MD=14.75, 95%CI 2.01 to 27.48, P=0.02). However, no significant difference was found between the two group in minor amputation rates (RR=0.70, 95%CI 0.24 to 2.11, P=0.53). In addition, neither relevant serious adverse reaction nor complications were reported when using hyperbaric oxygen therapy as adjunctive treatment.
ConclusionCurrent evidence shows that hyperbaric oxygen therapy as adjunctive treatment could improve ulcer healing and reduce incidence of major amputation.
OBJECTIVE To investigate clinical effects and possible mechanisms of various growth factors on impaired healing ulcers of patients with diabetic disease. METHODS Seventy-eight patients were divided into three groups; saline control, epidermal growth factor(EGF) experimental group, and platelet-derived wound healing factor (PDWHF) experimental group. General healing conditions, wound closing index, healing rates and histological changes of the patient’s ulcer wound were observed during 1-8 weeks after treatment. RESULTS The wound closing index and healing rate of ulcers were significantly increased in the EGF and PDWHF experimental groups compared with the control group, while the angiogenesis, fibroblast hyperplasia, and collagen deposit were more obvious in EGF and PDWHF experimental groups than that of control group. The promoting effects on wound healing in PDWHF experimental group were better than in EGF group. CONCLUSION It suggests that local application of certain growth factor alone or various growth factors together is an effective method to improve the condition of impaired healing of diabetic ulcers.
Objective To explore the situation and causes of misdiagnosed hypoglycemia in China so as to develop some strategies for reducing misdiagnosis.Methods We searched CBMdisc, CMCC, CJFD and VIP (Jan. 1994-Dec. 2003). All the publisled studies about the misdiagnosis of hypoglycemia were collected to analyse their classifications and causes.Results A total of 172 studies involving 1 478 patients met the inclusion criteria. The studies were either case reports or clinical reviews. The 1 478 cases were misdiagnosed as 31 sorts of diseases, mainly including stroke (71.18%), transient ischemia attack (4.87%), epilepsy (4.13%) and hepatic coma (2.64%) . The causes of misdiagnosis could be classified into 14 categories, including complex manifestations of hypoglycemia (29.07%), lack of knowledge of hypoglycemic encephalopathy (16.44%), insufficient medical history collection (10.21%) and interference of compound diseases (9.86%) etc..Conclusions The misdiagnosis of hypoglycemia is mainly caused by the poor professional skills of doctors or their lack of responsibility, and poor patient management, especially when hypoglycemia are manifested by brain disability.
Objective To observe the effect of intravitreal injection of mouse nerve growth factor (NGF) on interphotoreceptor retinoid-binding protein (IRBP) in the vitreous of diabetic rats at early stages. Methods Ninety-six male Sprague Dawley (SD) rats were divided into control group (group A, 24 rats) and experimental group (72 rats). The rats in experimental group were induced with streptozotocin injection for diabetic retinopathy model, and then randomly divided into positive control group (group B), normal saline group (group C) and NGF group (group D), 24 rats in each group. The rats in the group A and B were not intervened. The rats were received intravitreal injection with 4mu;l normal saline (group C) or 4 mu;l (0.5 mu;g/mu;l) NGF (group D). At 2, 4, 6 and 8 weeks after injection, IRBP levels were detected by enzymelinked immunosorbent assay (ELISA); hematoxylin-eosin (HE) staining and light microscope were used to observe the morphological changes of the retina; transmission electron microscope was used to observe the retinal ultrastructure.Results At 2 weeks after injection, there was no significant difference in IRBP expression between group A,B,C and D (F=2.833，P=0.052). At 4, 6, 8 weeks after injection, the differences of IRBP expression between group A, B, C and D were significant (F=22.252, 108.459, 105.726; P=0.000). At different time points after injection, there was no significant difference in IRBP expression of group A (F=1.462, P=0.241), but there were significant differences in IRBP expression of group B, C and D (F=150.98, 63.519, 64.604; P=0.000). Light microscope found that the retinal structure was clear in group A and in group B, C, D at 2, 4 weeks after injection; the retinal thickness were thinner in group B, C, D at 8 weeks after injection. Transmission electron microscope displayed that the structure of rod outer segments was clear in group A and in group B, C, D at 2 weeks after injection; partly unclear structure of rod outer segments and slightly enlarged gap were observed in group B, C, D at 4, 8 weeks after injection. Conclusion Intravitreal injection with NGF can stabilize the IRBP expression in the vitreous of diabetic rats at early stages effectively.
Objective To evaluate the effect of the local del ivery of basic fibroblast growth factor 2 (bFGF-2) on the osseointegration around titanium implant of diabetic rats. Methods The bFGF-2-loaded poly (lactic-co-glycol ic acid) microspheres were prepared by water/oil/water (W/O/W) double-emulsion solvent evaporation method. Thirty-five male SPF level Sprague Dawley rats, weighing 220-250 g and aged 9 weeks, were selected as experimental animals. Ten rats were fedwith the routine diet as normal control group. The other 25 rats were made the diabetic animal model by giving high fat-sugar diet and a low dose streptozotocin (30 mg/ kg) intravenously; 20 rats were made the diabetic animal model successfully. Then 20 rats were randomly divided into diabetic control group (n=10) and bFGF-2 intervention group (n=10). A hole was drilled in the right tibia bone of all rats, and the titanium implant treated by micro-arc oxidation surface was planted into the hole. Simultaneously, the previously prepared microspheres and blood were mixed and were loaded on the surface of the implant before it was implanted into the rats of the bFGF-2 intervention group. At 4 and 8 weeks, the tibia containing implants was harvested, embedded with resin and made undecalcified tissue sl ices to compare the osseointegration. Results At 4 weeks, the implants of the normal control group were surrounded by new lamellar bone with continuity; whereas the tissue around the implants of the diabetic control group contained l ittle woven bone and some fibrous tissue; and obvious new formed bone with continuity was observed in bFGF-2 intervention group. At 8 weeks, the results of 3 groups were similar to those at 4 weeks. At 4 weeks, the percentage of bone-implant contact (BIC) in diabetic control group was significantly less than those in normal control group (P lt; 0.05) and in bFGF-2 intervention group (P lt; 0.05); the BIC in bFGF-2 intervention group was less than in normal control group, but showing no significant difference (P gt; 0.05). After 8 weeks, the BIC in normal control group and in bFGF-2 intervention group were significantly greater than that in diabetic control group (P lt; 0.05), but there was no significant difference between bFGF-2 intervention group and normal control group (P gt; 0.05). Conclusion Local del ivery of bFGF-2 around titanium implants may improve the osseointegration in diabetic rats.
