The objective of this study was to examine the underlying factors and epidemiological traits of a cluster epidemic of cutaneous anthrax in Northern Anhui,to formulate targeted preventive and control strategies.After the epidemic,a rigorous epidemiological investigation was undertaken,including collection of clinical specimens and environmental samples for laboratory analysis.A total of 11 cutaneous anthrax cases were reported,comprising 2 confirmed,6 clinically diagnosed,and 3 suspected cases.These cases were geographically dispersed across a slaughterhouse in Yingzhou District,Fuyang City(5 ca-ses),and a village in Lixin County,Bozhou City(6 cases).All cases were in people engaged in cattle breeding,slaughtering,sales,and other work.The source of infection was traced to cattle purchased from a livestock trading market in another prov-ince.Our findings underscore that this epidemic was a locally transmitted,human-to-human outbreak stemming from the intro-duction of infected animals from another province.Notably,direct contact with infected cattle emerged as the primary mode of infection.

The objective of this study was to examine the underlying factors and epidemiological traits of a cluster epidemic of cutaneous anthrax in Northern Anhui,to formulate targeted preventive and control strategies.After the epidemic,a rigorous epidemiological investigation was undertaken,including collection of clinical specimens and environmental samples for laboratory analysis.A total of 11 cutaneous anthrax cases were reported,comprising 2 confirmed,6 clinically diagnosed,and 3 suspected cases.These cases were geographically dispersed across a slaughterhouse in Yingzhou District,Fuyang City(5 ca-ses),and a village in Lixin County,Bozhou City(6 cases).All cases were in people engaged in cattle breeding,slaughtering,sales,and other work.The source of infection was traced to cattle purchased from a livestock trading market in another prov-ince.Our findings underscore that this epidemic was a locally transmitted,human-to-human outbreak stemming from the intro-duction of infected animals from another province.Notably,direct contact with infected cattle emerged as the primary mode of infection.

It is well established that increased excitability of the presympathetic neurons in the hypothalamic paraventricular nucleus (PVN) during hypertension leads to heightened sympathetic outflow and hypertension. However, the mechanism underlying the overactivation of PVN presympathetic neurons remains unclear. This study aimed to investigate the role of endogenous corticotropin-releasing factor (CRF) on the excitability of presympathetic neurons in PVN using Western blot, arterial blood pressure (ABP) and renal sympathetic nerve activity (RSNA) recording, CRISPR/Cas9 technique and patch-clamp technique. The results showed that CRF protein expression in PVN was significantly upregulated in spontaneously hypertensive rats (SHRs) compared with normotensive Wistar-Kyoto (WKY) rats. Besides, PVN administration of exogenous CRF significantly increased RSNA, heart rate and ABP in WKY rats. In contrast, knockdown of upregulated CRF in PVN of SHRs inhibited CRF expression, led to membrane potential hyperpolarization, and decreased the frequency of current-evoked firings of PVN presympathetic neurons, which were reversed by incubation of exogenous CRF. Perfusion of rat brain slices with artificial cerebrospinal fluid containing CRF receptor 1 (CRFR1) blocker, NBI-35965, or CRF receptor 2 (CRFR2) blocker, Antisauvagine-30, showed that blocking CRFR1, but not CRFR2, hyperpolarized the membrane potential and inhibited the current-evoked firing of PVN presympathetic neurons in SHRs. However, blocking CRFR1 or CRFR2 did not affect the membrane potential and current-evoked firing of presympathetic neurons in WKY rats. Overall, these findings indicate that increased endogenous CRF release from PVN CRF neurons enhances the excitability of presympathetic neurons via activation of CRFR1 in SHRs.
Rats ; Animals ; Rats, Inbred SHR ; Paraventricular Hypothalamic Nucleus/physiology* ; Receptors, Corticotropin-Releasing Hormone/metabolism* ; Rats, Inbred WKY ; Corticotropin-Releasing Hormone/metabolism* ; Neurons/physiology* ; Hypertension ; Sympathetic Nervous System

In this study, we investigated the genetics, clinical features, and therapeutic approach of 14 patients with 5α-reductase deficiency in China. Genotyping analysis was performed by direct sequencing of PCR products of the steroid 5α-reductase type 2 gene (SRD5A2). The 5α-reductase activities of three novel mutations were investigated by mutagenesis and an in vitro transfection assay. Most patients presented with a microphallus, variable degrees of hypospadias, and cryptorchidism. Eight of 14 patients (57.1%) were initially reared as females and changed their social gender from female to male after puberty. Nine mutations were identified in the 14 patients. p.G203S, p.Q6X, and p.R227Q were the most prevalent mutations. Three mutations (p.K35N, p.H162P, and p.Y136X) have not been reported previously. The nonsense mutation p.Y136X abolished enzymatic activity, whereas p.K35N and p.H162P retained partial enzymatic activity. Topical administration of dihydrotestosterone during infancy or early childhood combined with hypospadia repair surgery had good therapeutic results. In conclusion, we expand the mutation profile of SRD5A2 in the Chinese population. A rational clinical approach to this disorder requires early and accurate diagnosis, especially genetic diagnosis.
3-Oxo-5-alpha-Steroid 4-Dehydrogenase/genetics* ; Adolescent ; Adult ; Asian People/genetics* ; Child ; Child, Preschool ; China ; Disorder of Sex Development, 46,XY/genetics* ; Follicle Stimulating Hormone/blood* ; Genitalia, Male/abnormalities* ; Humans ; Hypospadias/genetics* ; Luteinizing Hormone/blood* ; Male ; Membrane Proteins/genetics* ; Mutation/genetics* ; Sequence Alignment ; Steroid Metabolism, Inborn Errors/genetics* ; Testosterone/blood* ; Young Adult

Erectile dysfunction (ED) associated with type 2 diabetes is a severe problem that requires effective treatment. Pancreatic kininogenase (PK) has the potential to improve the erectile function of ED patients. This study aims to investigate the effect of PK on erectile function in streptozotocin-induced type 2 diabetic ED rats. To achieve this goal, we divided male Sprague-Dawley rats into five groups. One group was not treated, and the other four groups were treated with saline, sildenafil, PK or sildenafil, and PK, respectively, for 4 weeks after the induction of type 2 diabetic ED. Then, intracavernous pressure under cavernous nerve stimulation was measured, and penile tissue was collected for further study. Endothelial nitric oxide synthase levels, smooth muscle content, endothelium content, cyclic guanosine monophosphate (cGMP) levels in the corpus cavernosum, and neuronal nitric oxide synthase levels in the dorsal penile nerve were measured. Improved erectile function and endothelium and smooth muscle content in the corpus cavernosum were observed in diabetic ED rats. When treating diabetic ED rats with PK and sildenafil at the same time, a better therapeutic effect was achieved. These data demonstrate that intraperitoneal injection of PK can improve erectile function in a rat model of type 2 diabetic ED. With further research on specific mechanisms of erectile function improvement, PK may become a novel treatment for diabetic ED.
Animals ; Cyclic GMP/metabolism* ; Diabetes Mellitus, Experimental/physiopathology* ; Erectile Dysfunction/physiopathology* ; Kallikreins/therapeutic use* ; Male ; Muscle, Smooth, Vascular/physiopathology* ; Nitric Oxide Synthase Type I/metabolism* ; Nitric Oxide Synthase Type III/metabolism* ; Penile Erection/physiology* ; Penis/metabolism* ; Rats ; Rats, Sprague-Dawley ; Sildenafil Citrate/therapeutic use* ; Treatment Outcome ; Urological Agents/therapeutic use*

Amino Acid Metabolism, Inborn Errors ; genetics ; Female ; Glycine N-Methyltransferase ; deficiency ; genetics ; Humans ; Infant, Newborn ; Mutation

OBJECTIVETo investigate the molecular basis for a novel human leukocyte antigen (HLA) allele B*5827.

METHODSDNA from the proband was analyzed by polymerase chain reaction-sequence specific oligonucleotide (PCR-SSO) typing. The amplified product was sequenced bidirectionally.

RESULTSAbnormal HLA-B locus was observed and its nucleotide sequence was different from the known HLA-B allele sequences, with highest homology to HLA-B*5820 allele. It differs from HLA-B*5820 by 8 nucleotide substitutions in exon 3, i.e., nt 290 (G > C), nt 346 (T > A), nt 390 (A > C), nt 404 (G > C), nt 413 (C > G), nt 471 (A > G), nt 486 (A > G) and nt 487 (C > A), resulting in an amino acid change from ser > arg at nt 97, phe >tyr at nt 115, ser > arg at nt 130, thr > ala at nt 157 and thr > glu at nt 162. Nucleotide differences of nt 404 (G > C) and nt 413( C > G) did not change amino acid.

CONCLUSIONThe sequences of the novel allele have been submitted to GenBank (access No.GU071234). A novel HLA class I allele B*5827 has been officially assigned by the WHO HLA Nomenclature Committee in Jan. 2010.

Alleles ; Base Sequence ; Cloning, Molecular ; Genotype ; HLA-B Antigens ; chemistry ; genetics ; Humans ; Molecular Sequence Data ; Polymerase Chain Reaction ; Sequence Analysis, DNA

Objective To analyze the incidence of coronary artery disease (CAD) and outcome of patients with left ventricular noncompaction (LVNC). Methods Fifty-one patients with LVNC evaluated by echocardiography and/or cardiac magnetic resonance (CMR) from January 2006 to August 2010 were retrospectively reviewed. Coronary angiography or MDCT was performed for detecting coronary artery disease. Predictors of the cardiac events were analyzed by Cox regression analysis. Results There were 31 LVNC patients without CAD and 20 LVNC patients with CAD including single vessel coronary disease in 9 cases, double vessel coronary disease in 3 cases, three vessel coronary disease in 5 cases and left main coronary disease in 3 cases. Coronary artery bypass graft and percutaneous coronary intervention (PCI) were performed in 4 patients. Compared to LVNC patients without CAD, mean age ( P = 0. 008 ), incidence of hypertension (65.0% vs. 19. 4% , P = 0. 001 ), diabetes mellitus (40. 0% vs. 12. 9% , P = 0. 026) and hyperlipidemia ( 55.0% vs. 25. 8%, P = 0. 035 ) were significantly higher while NT-proBNP level was significantly lower( P = 0. 049 ) in LVNC patients with CAD. Incidence of major cardiac events was similar in LVNC patients with or without CAD. LogNT-proBNP is the independent prognostic factor for adverse cardiac events in patients with LVNC( HR 3.993,95% CI 1. 140-13. 988 ,P =0. 030). Conclusions Coronary artery disease is common in patients with LVNC and associated with traditional risk factors for CAD. Poor prognosis is associated with increased NT-proBNP but not with CAD in this patient cohort.

Objective To investigate the glycated hemoglobin Alc level (HbAlc) and its role in diagnosing impaired fasting glucose (IFG) and type 2 diabetes mellitus (T2DM) in civil pilots.Methods One hundred and fifty-one civil pilots,who were in routine physical examination in Civil Aviation General Hospital,were chosen as pilot group and 96 common examined personnel were taken as control group.The pilot goup was further analyzed by different HbAlc and FPG level to get the correlation between them.The level of fasting plasma glucose (FPG),lipid profiles,liver and renal function markers and HbAlc were measured and analyzed.Results No difference of HbAlc was observed between pilot and control group.The HbAlc levcl was significantly higher in IFG and T2DM sub-group than that in normal glucose sub-group (P＜0.01).The multiple linear regression analysis indicated that FPG,γ-glutamyl transferase (γ-GT),alanine transaminase (ALT),and serum creatinine (SCr) were the significant and independent influencing factors against HbAlc.The receiver operating characteristic (ROC) curve showed that HbAlc at the level of 5.6％ and 6.2％ was the best cut-off value for diagnosing and screening IFG and T2DM.Conclusions HbAlc may be the key indicator in diagnosing and monitoring IFG and T2DM,as well as in evaluating cardiovascular disease incidence for civil pilot.Besides routinely monitoring FPG in physical examination,HbAlc should be the indicator in assessing glucose metabolism for the pilot with T2DM and taking hypoglycemic drugs.

Objective To investigate the glycated hemoglobin Alc level (HbAlc) and its role in diagnosing impaired fasting glucose (IFG) and type 2 diabetes mellitus (T2DM) in civil pilots.Methods One hundred and fifty-one civil pilots,who were in routine physical examination in Civil Aviation General Hospital,were chosen as pilot group and 96 common examined personnel were taken as control group.The pilot goup was further analyzed by different HbAlc and FPG level to get the correlation between them.The level of fasting plasma glucose (FPG),lipid profiles,liver and renal function markers and HbAlc were measured and analyzed.Results No difference of HbAlc was observed between pilot and control group.The HbAlc levcl was significantly higher in IFG and T2DM sub-group than that in normal glucose sub-group (P＜0.01).The multiple linear regression analysis indicated that FPG,γ-glutamyl transferase (γ-GT),alanine transaminase (ALT),and serum creatinine (SCr) were the significant and independent influencing factors against HbAlc.The receiver operating characteristic (ROC) curve showed that HbAlc at the level of 5.6％ and 6.2％ was the best cut-off value for diagnosing and screening IFG and T2DM.Conclusions HbAlc may be the key indicator in diagnosing and monitoring IFG and T2DM,as well as in evaluating cardiovascular disease incidence for civil pilot.Besides routinely monitoring FPG in physical examination,HbAlc should be the indicator in assessing glucose metabolism for the pilot with T2DM and taking hypoglycemic drugs.