Analysis of Clinical Characteristics of 556 Spinal Tuberculosis Patients in Two Tertiary Teaching Hospitals in Guangxi Province.

Spinal tuberculosis (STB), which accounts for half of musculoskeletal tuberculosis, is among the leading causes of extrapulmonary tuberculosis. Guangxi Province, located in southern China, is among the most severely affected provinces in China. In this study, we collected and analyzed data from 2 Class-A tertiary teaching hospitals in Nanning City, Guangxi Province, from 2011 to 2019, with the aim of providing reference points for the prevention, diagnosis, treatment, and prognosis analysis of STB, using the epidemiological characteristics of 556 STB cases. Our results revealed that males had a slightly higher incidence (50.17%) compared to females (49.83%), with 64.93% of cases falling between the ages of 18 and 45 years. Cases from rural communities accounted for 63.49% of the reviewed cases. The average time between onset of symptoms and hospitalization was 18.0 months (range: 1 day-220 months). The most commonly reported symptoms were lower back pain (78.60%), radicular pain (51.98%), and systemic toxemia (43.53%). Additionally, 53.98% of the reviewed cases had varying degrees of neurological impairment. The main pathological lesion locations were the lumbar spine (43.53%) and thoracic spine (32.55%). Among them, 72.66% of cases involved at least 2 vertebral segments, and 62.77% of cases presented with paravertebral abscesses. Among the cases reviewed, 90.65% underwent antituberculosis chemotherapy prior to surgery. Following treatment, the cure rate was 78.41%, while 3.78% of patients had postoperative relapse. There were cases of concomitant illnesses among the cases reviewed, 40.65% of patients also had pulmonary tuberculosis, 15.29% had hepatitis B, 13.30% had diabetes, and 7.91% had hypertension. Our results still demonstrate that spinal tuberculosis remains a serious public health problem in Guangxi Province. Thus, preventive measures should be directed towards rural residents with comorbidities such as the elderly and diabetic.

Thymosin ß4 prevents oxygen-glucose deprivation/reperfusion-induced injury in rat cortical neurons.

PURPOSE: This study investigated whether thymosin (T) ß4 protects against oxygen-glucose deprivation/reperfusion (OGD/R) injury in rat cortical neurons, as well as the underlying mechanisms. METHODS: Primary rat cortical neurons were transfected with Tß4 overexpression plasmid; the transfection efficiency was confirmed by detecting Tß4 expression by fluorescence quantitative PCR and Western blotting. The OGD/R model was established and apoptotic cells were quantified by flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling. Structural changes in the endoplasmic reticulum were visualized by transmission electron microscopy. The expression levels of 78-kDa glucose-regulated protein (GRP) 78, C/EBP-homologous protein (CHOP), B-cell lymphoma (Bcl)-2, and Bcl-2-associated X protein (Bax) were determined by Western blotting. The effect of Tß4 on OGD/R injury was evaluated by adding exogenous Tß4 to neuronal cultures. RESULTS: Cortical neurons were identified by the expression of neuron-specific enolase. In OGD/R cells, the rate of apoptosis was increased and GRP78, CHOP, and Bax were upregulated whereas Bcl-2 was downregulated relative to the control group. These effects were reversed by Tß4 overexpression. Endoplasmic reticulum (ER) stress was observed in the OGD/R group, but this was abolished in neurons overexpressing Tß4. The protective effect of Tß4 against OGD/R injury was also demonstrated in cells treated with exogenous Tß4 (10 ng/mL), which blocked OGD/R-induced apoptosis by inhibiting ER stress-related and pro-apoptotic protein expression. CONCLUSION: Tß4 prevents OGD/R-induced ER stress-dependent apoptosis in cortical neurons, and is a potential treatment for cerebral ischemia-reperfusion injury.

Effects of thymosin ß4 on neuronal apoptosis in a rat model of cerebral ischemia­reperfusion injury.

The aim of the present study was to investigate the protective effects of thymosin ß4 (Tß4) on neuronal apoptosis in rat middle cerebral artery occlusion ischemia/reperfusion (MCAO I/R) injury, and determine the mechanisms involved in this process. Forty­eight adult male Sprague­Dawley rats were randomly divided into three groups (n=16 per group): A sham control group, an ischemia/reperfusion group (I/R group), and a Tß4 group. The focal cerebral I/R model was established by blocking the right MCA for 2 h, followed by reperfusion for 24 h. The Zea­Longa method was used to assess neurological deficits. Cerebral infarct volume was assessed using 2,3,5­triphenyltetrazolium chloride staining, and pathological changes were observed via hematoxylin and eosin staining. The terminal dexynucleotidyl transferase (TdT)­mediated dUTP nick end labeling (TUNEL) assay was used to detect apoptosis. The expression of glucose­regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), and caspase­12 (CASP12) protein was assessed using immunohistochemistry and western blotting 24 h after reperfusion. Infarct volume and neuronal damage in the I/R and Tß4 groups were significantly greater than those observed in the sham group. The Zea­Longa score, neuronal apoptosis, and expression of GRP78, CHOP, and CASP12 in the I/R and Tß4 groups were significantly higher than those reported in the sham group. However, the Longa score and neuronal apoptosis were lower in the Tß4 group compared to the I/R group. The expression of GRP78 was significantly increased, whereas that of CHOP and CASP12 was significantly decreased in the Tß4 group compared to the I/R group. The present data revealed that Tß4 can inhibit neuronal apoptosis by upregulating GRP78 and downregulating CHOP and CASP12, thereby reducing cerebral I/R injury.

Decreased leukocyte telomere length (LTL) is associated with stroke but unlikely to be causative.

AIMS: Interindividual variability in telomere length is highly heritable. Leukocyte telomere length (LTL) shortening has been shown to be associated with the process of atherosclerosis. But whether the inheritance of LTL is related to stroke is still unclear. The aim of this study was to test if telomere shortening was associated with stroke and whether this association was mainly due to inheritance or acquired cardiovascular risk factors. METHODS: Our study was focused on stroke in patients and their siblings. 450 subjects were recruited into this study: 150 patients with ischemic stroke as case group, 150 siblings of patients free of stroke (sibling group) and 150 healthy people as normal control. LTL was measured by real-time Polymerase Chain Reactions. The association between LTL and the cardiovascular risk factors was also determined. RESULTS: A significant decrease of LTL was found in case group when comparing with sibling (0.92±0.77 vs 1.68±1.24, p<0.001) and normal groups (0.92±0.77 vs 1.95±1.07, p<0.001), but no significant difference was found between sibling group and healthy control (p = 0.330). Shorter telomere length was independently associated with hypertension (p = 0.029, OR = 2.189, 95%CI:1.084-4.421), recent social pressure (p = 0.001, OR = 3.121, 95%CI:1.597-6.101), age (p = 0.004, OR = 1.055, 95%CI:1.017-1.093), HDL (p = 0.022, OR = 0.227, 95%CI:0.064-0.810) and diabetes (p = 0.018, OR = 3.174, 95%CI:1.221-8.252). Additionally, shortened length of telomere (p = 0.017, OR = 3.996, 95%CI:1.283-12.774) was an independent risk biomarker for stroke among case and sibling groups. CONCLUSION: The present study has demonstrated that decreased LTL might be associated with ischemic stroke but unlikely to be causative.